Liver sinusoidal endothelial cells in hepatic fibrosis

DeLeve, Laurie D.

doi:10.1002/hep.27376

Cited by 482Liver physiology and pathologyLiver Disease and TransplantationLiver Disease Diagnosis and Treatment

Liver sinusoidal endothelial cells in hepatic fibrosis

Open access

DeLeve, Laurie D.·2015·Hepatology

DOI 10.1002/hep.27376PMC PMC4333127

Open this paper in CoChat — free account

Abstract

Capillarization, lack of liver sinusoidal endothelial cell (LSEC) fenestration, and formation of an organized basement membrane not only precedes fibrosis, but is also permissive for hepatic stellate cell activation and fibrosis. Thus, dysregulation of the LSEC phenotype is a critical step in the fibrotic process. Both a vascular endothelial growth factor (VEGF)‐stimulated, nitric oxide (NO)‐independent pathway and a VEGF‐stimulated NO‐dependent pathway are necessary to maintain the differentiated LSEC phenotype. The NO‐dependent pathway is impaired in capillarization and activation of this pathway downstream from NO restores LSEC differentiation in vivo . Restoration of LSEC differentiation in vivo promotes HSC quiescence, enhances regression of fibrosis, and prevents progression of cirrhosis. (H epatology 2015;61:1740–1746)

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Integrity signals

Registry

Crossref · 10.1002/hep.27376

Cites

51 of 51 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

In healthy livers, LSECs prevent HSC activation.
“In healthy livers, LSECs prevent HSC activation [304].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [304]
Capillarized LSECs lose their HSC-suppressive properties and contribute to an environment that favors HSC activation and fibrosis.
“Capillarized LSECs (Fig. 4), characterized by high nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)-dependent collagen IV release [305], lose their HSC-suppressive properties and thereby contribute to an environment that favors HSC activation and fibrosis [304].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [304]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Myofibroblasts revert to an inactive phenotype during regression of liver fibrosis
Kisseleva, T., Cong, M., Paik, Y., Scholten, D., Jiang, C., Benner, C., Iwaisako, K., Moore-Morris, T., Scott, B., Tsukamoto, H., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1201840109 · Cited by 805 · cited 1× · see citing works
“In vivo studies have suggested that activated HSCs do not revert to full quiescence upon regression of fibrosis, but that HSCs that develop a quiescent phenotype after regression of fibrosis are poised to rapidly reactivate when challenged with a fibrotic stimulus.(47) These HSCs have been termed inactivated HSCs.”
Background
Efficient presentation of exogenous antigen by liver endothelial cells to CD8+ T cells results in antigen-specific T-cell tolerance
Limmer, A., Ohl, J., Kurts, C., Ljunggren, H.-G., Reiss, Y., Groettrup, M., Momburg, F., Arnold, B., & Knolle, P. A. (2000) · Nature Medicine · doi:10.1038/82161 · Cited by 758 · cited 1× · see citing works
“In normal liver, LSECs are tolerogenic (44, 45).”
Hepatic macrophages but not dendritic cells contribute to liver fibrosis by promoting the survival of activated hepatic stellate cells in mice
Pradere, J.-P., Kluwe, J., De Minicis, S., Jiao, J.-J., Gwak, G.-Y., Dapito, D. H., Jang, M.-K., Guenther, N. D., Mederacke, I., Friedman, R., et al. (2013) · Hepatology · doi:10.1002/hep.26429 · Cited by 613 · cited 1× · see citing works
“During chronic liver disease, Kupffer cells prevent HSC apoptosis and thereby sustain the fibrotic process.(51) Thus, there is an intricate interplay among the nonparenchymal cells that either prevents or sustains HSC activation and thereby determines fibrosis (Fig.”
Capillarization of hepatic sinusoids in man
Schaffner, F., & Popper, H. (1963) · Gastroenterology · doi:10.1016/s0016-5085(63)80130-4 · Cited by 610 · cited 1× · see citing works
“INTRODUCTION Capillarization, which is when liver sinusoidal endothelial cells (LSECs) lack fenestration and develop an organized basement membrane (1), is a prelude to fibrosis.”
Hypoxia-induced VEGF and collagen I expressions are associated with angiogenesis and fibrogenesis in experimental cirrhosis
Corpechot, C., Barbu, V. D., Wendum, D., Kinnman, N., Rey, C., Poupon, R. Y., Housset, C., & Rosmorduc, O. (2002) · Hepatology · doi:10.1053/jhep.2002.32524 · Cited by 480 · cited 1× · see citing works
“VEGF is upregulated in cirrhosis (33, 34), so that total VEGF is not rate limiting in this process.”
Expression of variant fibronectins in wound healing: cellular source and biological activity of the EIIIA segment in rat hepatic fibrogenesis.
Jarnagin, W. R., Rockey, D. C., Koteliansky, V., Wang, S. S., & Bissell, D. M. (1994) · The Journal of Cell Biology · doi:10.1083/jcb.127.6.2037 · Cited by 452 · cited 2× · see citing works
“LSECs in a bile duct ligation model make increased quantities of EIIIAfibronectin.(42) HSCs cultured on matrix conditioned by LSECs isolated from the bile duct ligation model show increased activation that is blocked by antibodies to EIIIA fibronectin.”
Background
LYVE-1 is not restricted to the lymph vessels: expression in normal liver blood sinusoids and down-regulation in human liver cancer and cirrhosis.
Carreira, C. M., Nasser, S. M., di Tomaso, E., Padera, T. P., Boucher, Y., Tomarev, S. I., & Jain, R. K. (2001) · PubMed · Cited by 449 · see citing works
Apoptotic Body Engulfment by a Human Stellate Cell Line Is Profibrogenic
Canbay, A., Taimr, P., Torok, N., Higuchi, H., Friedman, S., & Gores, G. J. (2003) · Laboratory Investigation · doi:10.1097/01.lab.0000069036.63405.5c · Cited by 417 · cited 1× · see citing works
“During resolution of fibrosis, the decline in activated HSC is due to both reversion to quiescence and apoptosis (28, 50).”
Role of Differentiation of Liver Sinusoidal Endothelial Cells in Progression and Regression of Hepatic Fibrosis in Rats
Xie, G., Wang, X., Wang, L., Wang, L., Atkinson, R. D., Kanel, G. C., Gaarde, W. A., & DeLeve, L. D. (2012) · Gastroenterology · doi:10.1053/j.gastro.2011.12.017 · Cited by 410 · see citing works
Self-citation
Sinusoidal endothelial cells prevent rat stellate cell activation and promote reversion to quiescence
DeLeve, L. D., Wang, X., & Guo, Y. (2008) · Hepatology · doi:10.1002/hep.22351 · Cited by 408 · cited 5× · see citing works
“Hepatocytes are unable to maintain HSC quiescence unless the culture medium is supplemented with an NO-donor, but it remains to be determined whether NO contributes to the paracrine effect of LSECs on HSC quiescence or whether other paracrine factors are necessary.(36) Our group and others have reported that NO produc…”
BackgroundMethodInfluentialSelf-citation
Reduced nitric oxide production by endothelial cells in cirrhotic rat liver: Endothelial dysfunction in portal hypertension
Rockey, D. C., & Chung, J. J. (1998) · Gastroenterology · doi:10.1016/s0016-5085(98)70487-1 · Cited by 408 · cited 2× · see citing works
“In cirrhosis, decreased production of NO by LSECs (31) and increased production of endothelin-1 by HSCs promotes contractility of HSCs (38) and”
In vivo and in vitro uptake and degradation of acetylated low density lipoprotein by rat liver endothelial, Kupffer, and parenchymal cells.
Nagelkerke, J. F., Barto, K. P., & van Berkel, T. J. (1983) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)44160-3 · Cited by 392 · cited 1× · see citing works
“The hyaluronan/scavenger receptor clears hyaluronan, chondroitin sulphate, formaldehyde treated serum albumin (FSA, used as a test ligand for scavenger receptor-mediated endocytosis (9-11)), procollagen type I and III N-terminal peptides, nidogen, acetylated and oxidized low density lipoprotein (12-14), plasma coagula…”
A Dendritic Cell–Specific Intercellular Adhesion Molecule 3–Grabbing Nonintegrin (Dc-Sign)–Related Protein Is Highly Expressed on Human Liver Sinusoidal Endothelial Cells and Promotes HIV-1 Infection
Bashirova, A. A., Geijtenbeek, T. B. H., van Duijnhoven, G. C. F., van Vliet, S. J., Eilering, J. B. G., Martin, M. P., Wu, L. J., Martin, T. D., Viebig, N. K., Knolle, P. A., et al. (2001) · The Journal of Experimental Medicine · doi:10.1084/jem.193.6.671 · Cited by 358 · cited 1× · see citing works
“SIGN; aka CD209L or DC-SIGN-related (DC SIGNR)] (19), and LYVE-1 (20, 21).”
Impaired endothelial nitric oxide synthase activity associated with enhanced caveolin binding in experimental cirrhosis in the rat
Shah, V. H., Törüner, M., Haddad, F., Cadelina, G. W., Papapetropoulos, A., Choo, K. K., Sessa, W. C., & Groszmann, R. J. (1999) · Gastroenterology · doi:10.1016/s0016-5085(99)70408-7 · Cited by 340 · cited 1× · see citing works
“In capillarization, eNOS protein is unchanged, but eNOS activity is diminished with low production of NO(31) due to increased binding to caveolin.(32) Thus, the VEGF-stimulated, NO-dependent pathway is impaired.”
Background
Stabilin-1 and -2 constitute a novel family of fasciclin-like hyaluronan receptor homologues
Politz, O., Gratchev, A. N., McCourt, P., Schledzewski, K., Guillot, P., Johansson, S., Svineng, G., Franke, P., Kannicht, C., Kzhyshkowska, J. G., et al. (2002) · Biochemical Journal · doi:10.1042/0264-6021:3620155 · Cited by 310 · see citing works
Atorvastatin lowers portal pressure in cirrhotic rats by inhibition of RhoA/Rho-kinase and activation of endothelial nitric oxide synthase
Trebicka, J., Hennenberg, M., Laleman, W., Shelest, N., Biecker, E., Schepke, M., Nevens, F., Sauerbruch, T., & Heller, J. (2007) · Hepatology · doi:10.1002/hep.21673 · Cited by 306 · cited 1× · see citing works
“In the bile duct ligation model, statins increase hepatic eNOS and PKG activity,(41) decrease HSC Rho-kinase activity, and reduce portal pressure with decreased intrahepatic resistance.(41) Statin-induced up-regulation of the transcription factor KLF2 in hepatic endothelial cells increases eNOS expression, presumably…”
Background
Induction of cytokine production in naive CD4+ T cells by antigen-presenting murine liver sinusoidal endothelial cells but failure to induce differentiation toward Th1 cells☆, ☆☆
KNOLLE, P., SCHMITT, E., JIN, S., GERMANN, T., DUCHMANN, R., HEGENBARTH, S., GERKEN, G., & LOHSE, A. (1999) · Gastroenterology · doi:10.1016/s0016-5085(99)70508-1 · Cited by 298 · cited 1× · see citing works
“In normal liver, LSECs are tolerogenic (44, 45).”
Rat liver sinusoidal endothelial cell phenotype is maintained by paracrine and autocrine regulation
DeLeve, L. D., Wang, X., Hu, L., McCuskey, M. K., & McCuskey, R. S. (2004) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00017.2004 · Cited by 296 · see citing works
Self-citation
Different fate in vivo of oxidatively modified low density lipoprotein and acetylated low density lipoprotein in rats. Recognition by various scavenger receptors on Kupffer and endothelial liver cells
van Berkel, T. J., de Rijke, Y. B., & Kruijt, J. K. (1991) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)52241-9 · Cited by 279 · cited 1× · see citing works
“The hyaluronan/scavenger receptor clears hyaluronan, chondroitin sulphate, formaldehyde treated serum albumin (FSA, used as a test ligand for scavenger receptor-mediated endocytosis (9-11)), procollagen type I and III N-terminal peptides, nidogen, acetylated and oxidized low density lipoprotein (12-14), plasma coagula…”
A new communication system between hepatocytes and sinusoidal endothelial cells in liver through vascular endothelial growth factor and Flt tyrosine kinase receptor family (Flt-1 and KDR/Flk-1).
Yamane, A., Seetharam, L., Yamaguchi, S., Gotoh, N., Takahashi, T., Neufeld, G., & Shibuya, M. (1994) · PubMed · Cited by 251 · see citing works
Simvastatin treatment improves liver sinusoidal endothelial dysfunction in CCl4 cirrhotic rats
Abraldeṣ, J. G., Rodrı́guez-Vilarrupla, A., Graupera, M., Zafra, C., García‐Calderó, H., García‐Pagán, J. C., & Bosch, J. (2007) · Journal of Hepatology · doi:10.1016/j.jhep.2007.01.020 · Cited by 245 · cited 1× · see citing works
“In cirrhotic liver, statins increase hepatic eNOS activity and cGMP levels.(40) In the bile duct ligation model, statins increase hepatic eNOS and PKG activity,(41) decrease HSC Rho-kinase activity, and reduce portal pressure with decreased intrahepatic resistance.”
Background
The transcription factor KLF2 mediates hepatic endothelial protection and paracrine endothelial–stellate cell deactivation induced by statins
Marrone, G., Russo, L., Rosado, E., Hide, D., García‐Cardeña, G., García‐Pagán, J. C., Bosch, J., & Gracia‐Sancho, J. (2012) · Journal of Hepatology · doi:10.1016/j.jhep.2012.08.026 · Cited by 244 · cited 2× · see citing works
“Our group and others have reported that NO produced by LSECs maintains HSC quiescence: in coculture of LSECs with HSCs, inhibition of eNOS by L-NAME blocks the ability of LSECs to maintain HSC quiescence.(36,37) However, the flaw in the interpretation of these studies is that LSECs cultured in the presence of L-NAME c…”
Background
The scavenger endothelial cell: a new player in homeostasis and immunity
Sørensen, K. K., McCourt, P., Berg, T., Crossley, C., Couteur, D. G. L., Wake, K., & Smedsrød, B. H. (2012) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00686.2011 · Cited by 233 · see citing works
Advanced glycation end products are eliminated by scavenger-receptor-mediated endocytosis in hepatic sinusoidal Kupffer and endothelial cells
Smedsrød, B. H., Melkko, J., Araki, N., Sano, H., & Horiuchi, S. (1997) · Biochemical Journal · doi:10.1042/bj3220567 · Cited by 225 · cited 1× · see citing works
“The hyaluronan/scavenger receptor clears hyaluronan, chondroitin sulfate, formaldehydetreated serum albumin (FSA, used as a test ligand for scavenger receptor-mediated endocytosis(9-11)), procollagen type I and III N-terminal peptides, nidogen, acetylated and oxidized low density lipoprotein,(12-14) plasma coagulation…”
Background
Stabilin-1 and −2 constitute a novel family of fasciclin-like hyaluronan receptor homologues
Politz, O., Gratchev, A. N., McCourt, P., et al. (2002) · Biochemical Journal · doi:10.1042/bj3620155 · Cited by 216 · cited 1× · see citing works
“The hyaluronan/scavenger receptor, SR-H (stabilin-1 and stabilin-2), is the main functional scavenger receptor on the LSEC (6-8).”
Alcoholic liver injury: Defenestration in noncirrhotic livers—a scanning electron microscopic study
Horn, T. D., Christoffersen, P., & Henriksen, J. H. (1987) · Hepatology · doi:10.1002/hep.1840070117 · Cited by 184 · cited 1× · see citing works
“In vivo, loss of the unique fenestrated phenotype has been shown to precede onset of fibrosis in alcoholic liver injury (22), non-alcoholic fatty liver disease (23), toxic liver injury (24), and the intragastric alcohol infusion model (DeLeve LD et al, unpublished observation).”
Microenvironmental Regulation of the Sinusoidal Endothelial Cell Phenotype In Vitro
March, S., Hui, E. E., Underhill, G. H., Khetani, S., & Bhatia, S. N. (2009) · Hepatology · doi:10.1002/hep.23085 · Cited by 163 · cited 3× · see citing works
“FcγIIb2 (CD32b or SE-1 (16)), clears immune complexes formed with Ig G (17).”
Characterization of a hyaluronan receptor on rat sinusoidal liver endothelial cells and its functional relationship to scavenger receptors
McCourt, P., Smedsrød, B. H., Melkko, J., & Johansson, S. (1999) · Hepatology · doi:10.1002/hep.510300521 · Cited by 144 · cited 1× · see citing works
“The hyaluronan/scavenger receptor, SR-H (stabilin-1 and stabilin-2), is the main functional scavenger receptor on the LSEC (6-8).”
Stabilin-1 and stabilin-2 are both directed into the early endocytic pathway in hepatic sinusoidal endothelium via interactions with clathrin/AP-2, independent of ligand binding
HANSEN, B., Longati, P., Elvevold, K., Nedredal, G. I., Schledzewski, K., Olsen, R. E., Falkowski, M., Kzhyshkowska, J. G., CARLSSON, F., & JOHANSSON, S. (2005) · Experimental Cell Research · doi:10.1016/j.yexcr.2004.09.017 · Cited by 144 · see citing works
Expression of stabilin-2, a novel fasciclin-like hyaluronan receptor protein, in murine sinusoidal endothelia, avascular tissues, and at solid/liquid interfaces
Falkowski, M., Schledzewski, K., Hansen, B., & Goerdt, S. (2003) · Histochemistry and Cell Biology · doi:10.1007/s00418-003-0585-5 · Cited by 139 · cited 1× · see citing works
“used to identify LSECs include the expression of FcγIIb2 (17) (CD32b or anti-SE1 (16)), stabilin-2 (3, 18), liver/lymph node-specific ICAM-3-grabbing integrin [L-”
Hedgehog signalling regulates liver sinusoidal endothelial cell capillarisation
Xie, G., Choi, S. S., Syn, W., Michelotti, G. A., Swiderska, M., Karaca, G., Chan, I. S., Chen, Y., & Diehl, A. M. (2012) · Gut · doi:10.1136/gutjnl-2011-301494 · Cited by 133 · cited 1× · see citing works
“Hedgehog signaling is increased in LSECs that have capillarized in vitro and inhibition of hedgehog signaling blocks culture-induced capillarization.(35) It remains to be determined experimentally how the two pathways linked to capillarization, i.”
Background
Clearance of acetyl low density lipoprotein by rat liver endothelial cells. Implications for hepatic cholesterol metabolism.
Blomhoff, R., Drevon, C. A., Eskild, W., HELGERUD, P., Norum, K. R., & Berg, T. (1984) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)47239-5 · Cited by 126 · cited 1× · see citing works
“The hyaluronan/scavenger receptor clears hyaluronan, chondroitin sulphate, formaldehyde treated serum albumin (FSA, used as a test ligand for scavenger receptor-mediated endocytosis (9-11)), procollagen type I and III N-terminal peptides, nidogen, acetylated and oxidized low density lipoprotein (12-14), plasma coagula…”
Enhanced vasoconstrictor prostanoid production by sinusoidal endothelial cells increases portal perfusion pressure in cirrhotic rat livers
Gracia-Sancho, J., Laviña, B., Rodríguez-Vilarrupla, A., García-Calderó, H., Bosch, J., & García-Pagán, J. C. (2007) · Journal of Hepatology · doi:10.1016/j.jhep.2007.03.014 · Cited by 125 · cited 1× · see citing works
“In cirrhosis, decreased production of NO by LSECs(31) and increased production of endothelin-1 by HSCs promotes contractility of HSCs(38) and increased production of prostanoids by LSECs increases portal pressure.(39) Fig.”
Background
The mannose receptor on murine liver sinusoidal endothelial cells is the main denatured collagen clearance receptor
Malovic, I., Sφrensen, K. K., Elvevold, K., Nedredal, G. I., Paulsen, S. M., Erofeev, A. V., Smedsrød, B. H., & McCourt, P. (2007) · Hepatology · doi:10.1002/hep.21639 · Cited by 122 · cited 1× · see citing works
“, denatured collagen of several types of collagen, and glycoconjugates with terminal mannose, such as lysosomal enzymes, procollagen type I carboxyterminal propeptides, and tissue type plasminogen activator.(4,5) The hyaluronan/scavenger receptor, SR-H (stabilin-1 and stabilin-2), is the main functional scavenger rece…”
Background
Differential expression of a gene signature for scavenger/lectin receptors by endothelial cells and macrophages in human lymph node sinuses, the primary sites of regional metastasis
Martens, J., Kzhyshkowska, J. G., Falkowski, M., Schledzewski, K., Gratchev, A. N., Mansmann, U., Schmuttermaier, C., Dippel, E., Koenen, W., Riedel, F., et al. (2006) · The Journal of Pathology · doi:10.1002/path.1921 · Cited by 119 · see citing works
Nitrovasodilators inhibit platelet-derived growth factor-induced proliferation and migration of activated human hepatic stellate cells
Failli, P., DeFranco, R., Caligiuri, A., Gentilini, A., Romanelli, R. G., Marra, F., Batignani, G., Guerra, C. T., Laffi, G., Geñtilini, P., et al. (2000) · Gastroenterology · doi:10.1053/gast.2000.9354 · Cited by 118 · see citing works
In Hepatic Fibrosis, Liver Sinusoidal Endothelial Cells Acquire Enhanced Immunogenicity
Connolly, M. K., Bedrosian, A. S., Malhotra, A., Henning, J. R., Ibrahim, J., Vera, V., Cieza-Rubio, N. E., Hassan, B. U., Pachter, H., Cohen, S. M., et al. (2010) · Journal of Immunology · doi:10.4049/jimmunol.1000332 · Cited by 115 · cited 1× · see citing works
“However, in fibrosis, LSECs isolated from fibrotic liver secrete proinflammatory cytokines and chemokines and induce immunogenic T cells ex vivo.(46) If confirmed in vivo, this would suggest that capillarized LSECs might promote HSC activation.”
Background
Prevention of Hepatic Fibrosis in a Murine Model of Metabolic Syndrome with Nonalcoholic Steatohepatitis
DeLeve, L. D., Wang, X., Kanel, G. C., Atkinson, R., & McCuskey, R. S. (2008) · American Journal Of Pathology · doi:10.2353/ajpath.2008.070720 · Cited by 115 · see citing works
Self-citation
Receptor-mediated endocytosis of immune complexes in rat liver sinusoidal endothelial cells is mediated by FcγRIIb2
Mousavi, S. A., Sporstφl, M., Fladeby, C., Kjeken, R., Barois, N., & Berg, T. (2007) · Hepatology · doi:10.1002/hep.21748 · Cited by 113 · cited 2× · see citing works
“FcγIIb2 (CD32b or SE-1 (16)), clears immune complexes formed with Ig G (17).”
Endocytosis of formaldehyde-treated serum albumin via scavenger pathway in liver endothelial cells
Blomhoff, R., Eskild, W., & Berg, T. (1984) · Biochemical Journal · doi:10.1042/bj2180081 · Cited by 112 · cited 1× · see citing works
“The hyaluronan/scavenger receptor clears hyaluronan, chondroitin sulphate, formaldehyde treated serum albumin (FSA, used as a test ligand for scavenger receptor-mediated endocytosis (9-11)), procollagen type I and III N-terminal peptides, nidogen, acetylated and oxidized low density lipoprotein (12-14), plasma coagula…”
Liver sinusoidal endothelium: a microenvironment-dependent differentiation program in rat including the novel junctional protein liver endothelial differentiation-associated protein-1
Géraud, C., Schledzewski, K., Demory, A., Klein, D., Kaus, M., Peyre, F., Sticht, C., Evdokimov, K., Lu, S., Schmieder, A., et al. (2010) · Hepatology · doi:10.1002/hep.23618 · Cited by 109 · cited 1× · see citing works
“Both fenestration and endocytosis persist longer in vitro in the right microenvironment.(26,27) Vascular endothelial growth factor (VEGF), derived from hepatocytes and hepatic stellate cells, is a key regulator of the LSEC phenotype, as demonstrated both in vitro and in vivo.”
Background
Nitric Oxide-independent Activation of Soluble Guanylate Cyclase by BAY 60-2770 in Experimental Liver Fibrosis
Knorr, A., Hirth‐Dietrich, C., Alonso‐Alija, C., Härter, M. W., Hahn, M. G., Keim, Y., Wunder, F., & Stasch, J. (2011) · Arzneimittelforschung · doi:10.1055/s-0031-1296471 · Cited by 93 · cited 1× · see citing works
“This particular sGC activator prevents HSC activation in vitro (28) and prevents hepatic fibrosis if given simultaneously with the fibrotic stimulus (48).”
Regulation of Endothelin-1 Synthesis by Endothelin-converting Enzyme-1 during Wound Healing
Shao, R., Yan, W., & Rockey, D. C. (1999) · Journal of Biological Chemistry · doi:10.1074/jbc.274.5.3228 · Cited by 92 · cited 1× · see citing works
“In cirrhosis, decreased production of NO by LSECs (31) and increased production of endothelin-1 by HSCs promotes contractility of HSCs (38) and”
Development of murine hepatic sinusoidal endothelial cells characterized by the expression of hyaluronan receptors
Nonaka, H., Tanaka, M., Suzuki, K., & Miyajima, A. (2007) · Developmental Dynamics · doi:10.1002/dvdy.21227 · Cited by 84 · cited 2× · see citing works
“Markers that have been used to identify LSECs include the expression of FccIIb2 17 (CD32b or anti-SE-116), stabilin-2,3,18 liver/lymph node-specific ICAM-3-grabbing integrin [L-SIGN; aka CD209L or DC-SIGN-related (DC SIGNR),19 and LYVE-1.”
Evaluation of hyaluronic acid binding ability of hepatic sinusoidal endothelial cells in rats with liver cirrhosis
Tamaki, S., Ueno, T., Torimura, T., Sata, M., & Tanikawa, K. (1996) · Gastroenterology · doi:10.1016/s0016-5085(96)70074-4 · Cited by 75 · cited 1× · see citing works
“Endocytosis is impaired in capillarization (25), but there is not yet published evidence that the decline in endocytotic capacity precedes fibrosis or a comprehensive description of which endocytotic receptors are affected in capillarization.”
Isolation of periportal, midlobular, and centrilobular rat liver sinusoidal endothelial cells enables study of zonated drug toxicity
Xie, G., Wang, L., Wang, X., Wang, L., & DeLeve, L. D. (2010) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00302.2010 · Cited by 74 · cited 1× · see citing works
“Note that periportal LSECs (top panel) have fewer fenestrae per sieve plate (average 8 fenestrae per sieve plate), but larger fenestrae than centrilobular LSECs (average 24 fenestrae per sieve plate; middle panel).(2) Smaller, nonclustered holes are endocytic vesicles.”
BackgroundSelf-citation
Preparation of isolated liver endothelial cells and Kupffer cells in high yield by means of an enterotoxin
Blomhoff, R., Smedsrød, B. H., Eskild, W., Granum, P. E., & Berg, T. (1984) · Experimental Cell Research · doi:10.1016/0014-4827(84)90714-6 · Cited by 67 · cited 1× · see citing works
“The hyaluronan/scavenger receptor clears hyaluronan, chondroitin sulphate, formaldehyde treated serum albumin (FSA, used as a test ligand for scavenger receptor-mediated endocytosis (9-11)), procollagen type I and III N-terminal peptides, nidogen, acetylated and oxidized low density lipoprotein (12-14), plasma coagula…”
A Transgenic Model for Conditional Induction and Rescue of Portal Hypertension Reveals a Role of VEGF-Mediated Regulation of Sinusoidal Fenestrations
May, D., Djonov, V., Zamir, G. A., Bala, M., Safadi, R., Sklair‐Levy, M., & Keshet, E. (2011) · PLoS ONE · doi:10.1371/journal.pone.0021478 · Cited by 54 · cited 1× · see citing works
“Similarly, conditional induction of a VEGF decoy receptor that sequesters VEGF and precludes VEGF signaling leads to loss of LSEC fenestration.(29) After early cirrhosis is induced in an experimental model of toxin-induced parenchymal fibrosis, the thioacetamide model, a 1-week treatment with sGC activator, normalizes…”
Background
Fibronectin Extra Domain-A Promotes Hepatic Stellate Cell Motility but Not Differentiation Into Myofibroblasts
Olsen, A. L., Sackey, B. K., Marcinkiewicz, C., Boettiger, D. C., & Wells, R. G. (2011) · Gastroenterology · doi:10.1053/j.gastro.2011.12.038 · Cited by 49 · cited 2× · see citing works
“However, recent studies suggest that EIIIA fibronectin does not play an essential role in HSC activation in vitro or in vivo, but does contribute to HSC motility.(43) The effect on HSC may contribute to a modest profibrotic effect of EIIIA in a toxin-induced model of parenchymal fibrosis, but EIIIA does not appear to…”
Background
Intracellular transport of formaldehyde-treated serum albumin in liver endothelial cells after uptake via scavenger receptors
Eskild, W., Kindberg, G. M., Smedsrød, B. H., Blomhoff, R., Norum, K. R., & Berg, T. (1989) · Biochemical Journal · doi:10.1042/bj2580511 · Cited by 45 · cited 1× · see citing works
“The hyaluronan/scavenger receptor clears hyaluronan, chondroitin sulphate, formaldehyde treated serum albumin (FSA, used as a test ligand for scavenger receptor-mediated endocytosis (9-11)), procollagen type I and III N-terminal peptides, nidogen, acetylated and oxidized low density lipoprotein (12-14), plasma coagula…”
Cyclooxygenase-2 and vascular endothelial growth factor in chronic hepatitis, cirrhosis and hepatocellular carcinoma
Kwon, S. H., Jeong, S. W., Jang, J. Y., Lee, J. E., Lee, S. H., Kim, S. G., Kim, Y. S., Cho, Y. D., Kim, H. S., Kim, B. S., et al. (2012) · Clinical and Molecular Hepatology · doi:10.3350/cmh.2012.18.3.287 · Cited by 18 · cited 1× · see citing works
“VEGF is upregulated in cirrhosis (33, 34), so that total VEGF is not rate limiting in this process.”

Flagged first, then by citations

Sorted by citations

Single cell RNA sequencing of human liver reveals distinct intrahepatic macrophage populations
MacParland, S. A., Liu, J. C., Ma, X.-Z., Innes, B. T., Bartczak, A. M., Gage, B. K., Manuel, J., Khuu, N., Echeverri, J., Linares, I., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-06318-7 · Cited by 1,552 · see citing works
Liver sinusoidal endothelial cells: Physiology and role in liver diseases
Poisson, J., Lemoinne, S., Boulanger, C., Durand, F., Moreau, R., Valla, D., & Rautou, P.-E. (2017) · Journal of Hepatology · doi:10.1016/j.jhep.2016.07.009 · Cited by 1,047 · see citing works
“This distribution could be related to the progressive decrease in oxygen tension along the lobule accompanied with an increasing need for oxygen exchange [36].”
Background
Angiocrine functions of organ-specific endothelial cells
Rafii, S., Butler, J. M., & Ding, B. (2016) · Nature · doi:10.1038/nature17040 · Cited by 948 · see citing works
Pathobiology of liver fibrosis: a translational success story
Lee, Y. A., Wallace, M. C., & Friedman, S. L. (2015) · Gut · doi:10.1136/gutjnl-2014-306842 · Cited by 894 · see citing works
Organotypic vasculature: From descriptive heterogeneity to functional pathophysiology
Augustin, H. G., & Koh, G. Y. (2017) · Science · doi:10.1126/science.aal2379 · Cited by 762 · see citing works
“Fibrosis and HCC lead to LSEC transdifferentiation with loss of LSEC markers and sinusoidal fenestrae, a process known as capillarization, during which LSECs lose their protective properties andpromote angiogenesis and vasoconstriction (120, 121).”
Background
2016 Comprehensive Update of the Banff Working Group on Liver Allograft Pathology: Introduction of Antibody-Mediated Rejection
Demetris, A. J., Bellamy, C. O. C., Hübscher, S. G., O’Leary, J. G., Randhawa, P. S., Feng, S., Neil, D., Colvin, R. B., McCaughan, G. W., Fung, J. J., et al. (2016) · American Journal of Transplantation · doi:10.1111/ajt.13909 · Cited by 654 · see citing works
Liver sinusoidal endothelial cells — gatekeepers of hepatic immunity
Shetty, S., Lalor, P. F., & Adams, D. H. (2018) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-018-0020-y · Cited by 523 · see citing works
“Many studies have implicated vascular endothelial growth factor (VEGF) as an essential factor for regulation of fenestrations 21 , but dynamic changes in hepatic fenestration number and size can occur rapidly in response to agents such as alcohol 22 , diet ary constituents 23 and fasting 24 or calorie restriction 25 .”
BackgroundInfluential
The Power of Plasticity—Metabolic Regulation of Hepatic Stellate Cells
Trivedi, P., Wang, S., & Friedman, S. L. (2021) · Cell Metabolism · doi:10.1016/j.cmet.2020.10.026 · Cited by 427 · see citing works
“They also support sinusoidal endothelial cell integrity through paracrine interactions, which in turn are critical for angiogenesis during repair and regeneration (DeLeve, 2013, 2015; Desroches-Castan et al., 2019).”
Background
Hepatic fibrosis 2022: Unmet needs and a blueprint for the future
Friedman, S. L., & Pinzani, M. (2022) · Hepatology · doi:10.1002/hep.32285 · Cited by 430 · see citing works
Tumor restriction by type I collagen opposes tumor-promoting effects of cancer-associated fibroblasts
Bhattacharjee, S., Hamberger, F., Ravichandra, A., Miller, M., Nair, A., Affo, S., Filliol, A., Chin, L., Savage, T. M., Yin, D., et al. (2021) · Journal of Clinical Investigation · doi:10.1172/jci146987 · Cited by 367 · see citing works
“The strong interaction between HSC and endothelial cells, as observed in our CellPhoneDB analysis, is well recognized for normal and diseased liver (37).”
Background
Autophagy in liver diseases: A review
Qian, H., Chao, X., Williams, J. A. R., Fulte, S., Li, T., Yang, L., & Ding, W. (2021) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2021.100973 · Cited by 377 · see citing works
Role of liver sinusoidal endothelial cells in non-alcoholic fatty liver disease
Hammoutene, A., & Rautou, P.-E. (2019) · Journal of Hepatology · doi:10.1016/j.jhep.2019.02.012 · Cited by 364 · see citing works
Hepatocyte mitochondria-derived danger signals directly activate hepatic stellate cells and drive progression of liver fibrosis
An, P., Wei, L.-L., Zhao, S., Sverdlov, D. Y., Vaid, K. A., Miyamoto, M., Kuramitsu, K., Lai, M., & Popov, Y. V. (2020) · Nature Communications · doi:10.1038/s41467-020-16092-0 · Cited by 319 · see citing works
Hallmarks of Aging in the Liver
Hunt, N. J., Kang, S. W., Lockwood, G. P., Couteur, D. G. L., & Cogger, V. C. (2019) · Computational and Structural Biotechnology Journal · doi:10.1016/j.csbj.2019.07.021 · Cited by 315 · see citing works
Recent Advances in Understanding of Pathogenesis of Alcohol-Associated Liver Disease
Wu, X., Fan, X., Miyata, T., Kim, A., Cajigas-Du Ross, C. K., Ray, S., Huang, E., Taiwo, M., Arya, R., Wu, J., et al. (2023) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathmechdis-031521-030435 · Cited by 289 · see citing works
“The lack of a basement membrane contributes to the permissive nature of sinusoidal endothelium (96), allowing the LSECs and KCs to endocytically take up and eliminate invading pathogens (97).”
Background
Impaired endothelial autophagy promotes liver fibrosis by aggravating the oxidative stress response during acute liver injury
Ruart, M., Chavarria, L., Campreciós, G., Suárez-Herrera, N., Montironi, C., Guixé‐Muntet, S., Bosch, J., Friedman, S. L., García‐Pagán, J. C., & Hernández–Gea, V. (2018) · Journal of Hepatology · doi:10.1016/j.jhep.2018.10.015 · Cited by 286 · see citing works
Liver fibrosis: Pathophysiology and clinical implications
Berumen, J. A., Baglieri, J., Kisseleva, T., & Mekeel, K. L. (2020) · WIREs Mechanisms of Disease · doi:10.1002/wsbm.1499 · Cited by 262 · see citing works
“Moreover, following disruption of the endothelium, LSECs will secrete profibrogenic cytokines like TGF-β1, PDGF, interleukins, tumor necrosis factor α (TNFα), and VEGF, which will recruit inflammatory cells to the site of injury and activate HSCs (DeLeve, 2015).”
Background
Liver Sinusoidal Endothelial Cells
Sørensen, K. K., Simón-Santamaría, J., McCuskey, R. S., & Smedsrød, B. H. (2015) · Comprehensive physiology · doi:10.1002/cphy.c140078 · Cited by 257 · see citing works
Evolution in the understanding of the pathophysiological basis of portal hypertension: How changes in paradigm are leading to successful new treatments
Bosch, J., Groszmann, R. J., & Shah, V. H. (2015) · Journal of Hepatology · doi:10.1016/j.jhep.2015.01.003 · Cited by 252 · see citing works
“Recent work suggests that these changes may play a very important pathogenic role in the subsequent steps of liver fibrosis and highlight the potential role of the sinusoidal endothelial cell as a very early player, not only in increased intrahepatic resistance, but in liver injury and fibrosis itself [28,46].”
Alcoholic Liver Disease: Alcohol Metabolism, Cascade of Molecular Mechanisms, Cellular Targets, and Clinical Aspects
Teschke, R. (2018) · Biomedicines · doi:10.3390/biomedicines6040106 · Cited by 244 · see citing works
“LSECs are continuously exposed to the blood of the liver sinusoids, since they form their walls [276].”
Background
Size, shape, charge and “stealthy” surface: Carrier properties affect the drug circulation time in vivo
Di, J., Gao, X., Du, Y. L., Zhang, H., Gao, J., & Zheng, A. (2020) · Asian Journal of Pharmaceutical Sciences · doi:10.1016/j.ajps.2020.07.005 · Cited by 231 · see citing works
Diabetes mellitus in patients with cirrhosis: clinical implications and management
Elkrief, L., Rautou, P., Sarin, S. K., Valla, D. C., Paradis, V., & Moreau, R. (2016) · Liver International · doi:10.1111/liv.13115 · Cited by 222 · see citing works
“This mechanism is implicated in the progression of liver fibrosis (30).”
Background
Single-Cell Transcriptomics Reveals Zone-Specific Alterations of Liver Sinusoidal Endothelial Cells in Cirrhosis
Su, T., Yang, Y., Lai, S., Jeong, J., Jung, Y., McConnell, M., Utsumi, T., & Iwakiri, Y. (2021) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2020.12.007 · Cited by 220 · see citing works
“We also re-evaluated representative markers associated with these phenotypic alterations of LSECs.”
BackgroundInfluential
Regardless of etiology, progressive renal disease causes ultrastructural and functional alterations of peritubular capillaries
Bábíčková, J., Klinkhammer, B. M., Buhl, E. M., Djudjaj, S., Hoß, M., Heymann, F., Tacke, F., Floege, J., Becker, J. U., & Boor, P. (2016) · Kidney International · doi:10.1016/j.kint.2016.07.038 · Cited by 195 · see citing works
Liver fibrosis: from basic science towards clinical progress, focusing on the central role of hepatic stellate cells
Akkız, H., Gieseler, R. K., & Canbay, A. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25147873 · Cited by 191 · see citing works
“They play an important role in the secretion of vasoactive molecules, such as nitric oxide (NO) [113].”
Background
A defect in endothelial autophagy occurs in patients with non-alcoholic steatohepatitis and promotes inflammation and fibrosis
Hammoutene, A., Biquard, L., Lasselin, J., Kheloufi, M., Tanguy, M., Vion, A.-C., Mérian, J., Colnot, N., Loyer, X., Tedgui, A., et al. (2020) · Journal of Hepatology · doi:10.1016/j.jhep.2019.10.028 · Cited by 188 · see citing works
The evolving role of liver sinusoidal endothelial cells in liver health and disease
McConnell, M. J., Kostallari, E., Ibrahim, S. H., & Iwakiri, Y. (2023) · Hepatology · doi:10.1097/hep.0000000000000207 · Cited by 189 · see citing works
“These changes are thought to cause activation of HSCs, and thereby liver fibrosis/cirrhosis progression(6, 7).”
Pathological angiogenesis and inflammation in tissues
Jeong, J.-H., Ojha, U., & Lee, Y. M. (2020) · Archives of Pharmacal Research · doi:10.1007/s12272-020-01287-2 · Cited by 176 · see citing works
“However, in pathological conditions, they become capillarized (loss of fenestration), promote angiogenesis, and are unable to maintain the hepatic stellate cells in a quiescent state that contributes to fibrosis, inflammation and other chronic liver diseases (DeLeve 2015; Poisson et al.”
Background
Mechanotransduction-modulated fibrotic microniches reveal the contribution of angiogenesis in liver fibrosis
Liu, L., You, Z., Yu, H., Zhou, L., Zhao, H., Yan, X., Li, D., Wang, B., Zhu, L., Xu, Y., et al. (2017) · Nature Materials · doi:10.1038/nmat5024 · Cited by 163 · see citing works
GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis
Géraud, C., Reiners-Koch, P.-S., Zierow, J., Klapproth, K., Busch, K., Olsavszky, V., Leibing, T., Demory, A., Ulbrich, F., Diett, M., et al. (2017) · Journal of Clinical Investigation · doi:10.1172/jci90086 · Cited by 163 · see citing works
“, transdifferentiation of the liver microvasculature, is involved in metabolic and cirrhotic liver diseases as well as liver cancer and metastases (20, 21).”
Background
Endothelial Notch activation reshapes the angiocrine of sinusoidal endothelia to aggravate liver fibrosis and blunt regeneration in mice
Duan, J., Ruan, B., Yan, X., Liang, L., Song, P., Yang, Z., Liu, Y., Dou, K., Han, H., & Wang, L. (2018) · Hepatology · doi:10.1002/hep.29834 · Cited by 153 · see citing works
“HEPATOLOGY, Vol. , No. 2, 201868 damage, LSEC dedifferentiation promotes liver fibrogenesis, as demonstrated by many studies, likely through increased HSC activation attributed to upregulation of TGF-b and PDGFb.(10-13) Notch activation-induced LSEC dedifferentiation could be attributed to attenuated eNOS-sGC signalin…”
Background
BMP-9 interferes with liver regeneration and promotes liver fibrosis
Breitkopf‐Heinlein, K., Meyer, C., König, C., Gaitantzi, H., Addante, A., Thomas, M., Wiercinska, E., Cai, C., Li, Q., Wan, F., et al. (2017) · Gut · doi:10.1136/gutjnl-2016-313314 · Cited by 150 · see citing works
The Endothelium as a Driver of Liver Fibrosis and Regeneration
Lafoz, E., Ruart, M., Anton, A., Oncins, A., & Hernández–Gea, V. (2020) · Cells · doi:10.3390/cells9040929 · Cited by 147 · see citing works
“Therefore VEGF may have a dual role in fibrosis; it is essential in maintaining LSEC physiological phenotype through NO regulation [250] during fibrosis onset and promote reversion of HSC activated phenotype, ameliorating LSEC dysfunction during fibrosis resolution [12].”
Background
Immunofluorescence identifies distinct subsets of endothelial cells in the human liver
Strauss, O., Phillips, A., Ruggiero, K., Bartlett, A., & Dunbar, P. (2017) · Scientific Reports · doi:10.1038/srep44356 · Cited by 134 · see citing works
“A further investigation of the microanatomy of the liver lobule using vascular reconstruction in mice by Matsumoto and Kawakami 23 revealed a more accurate vascular distribution of zones that closely represents the staining patterns of Type 1 and Type 2 LSEC (see Figs 2 and 3).”
Mechanisms of organ fibrosis: Emerging concepts and implications for novel treatment strategies
Lurje, I., Gaisa, N. T., Weiskirchen, R., & Tacke, F. (2023) · Molecular Aspects of Medicine · doi:10.1016/j.mam.2023.101191 · Cited by 147 · see citing works
Role of immune responses in the development of NAFLD-associated liver cancer and prospects for therapeutic modulation
Yahoo, N., Dudek, M., Knolle, P. A., & Heikenwälder, M. F. (2023) · Journal of Hepatology · doi:10.1016/j.jhep.2023.02.033 · Cited by 145 · see citing works
Hepatic sinusoids in liver injury, inflammation, and fibrosis: new pathophysiological insights
Greuter, T., & Shah, V. H. (2016) · Journal of Gastroenterology · doi:10.1007/s00535-016-1190-4 · Cited by 139 · see citing works
“Besides the canonical pathway of constitutive expression of NO in SEC and its role in the quiescence of HSC [1, 19], numerous paracrine and autocrine factors and SEC/HSC crosstalk mechanisms have been identified and discussed in other reviews [1, 9, 20, 21].”
BackgroundInfluential
Endothelial Cell Dysfunction and Nonalcoholic Fatty Liver Disease (NAFLD): A Concise Review
Ansari, N. N., Ανδρουτσάκος, Θ., Flessa, C., Kyrou, I., Siasos, G., Randeva, H. S., Kassi, E. N., & Papavassiliou, A. G. (2022) · Cells · doi:10.3390/cells11162511 · Cited by 134 · see citing works
“LSEC capillarization occurs before KC activation and is permissive of hepatic stellate cell activation and the progression of inflammation and fibrosis [8,79,84].”
Background
Exosomes from activated hepatic stellate cells contain GLUT1 and PKM2: a role for exosomes in metabolic switch of liver nonparenchymal cells
Wan, L., Xia, T., Du, Y.-Q., Liu, J., Xie, Y.-Y., Zhang, Y.-J., Guan, F., Wu, J., Wang, X.-C., & Shi, C.-W. (2019) · The FASEB Journal · doi:10.1096/fj.201802675r · Cited by 118 · see citing works
Bone Morphogenetic Protein 9 Is a Paracrine Factor Controlling Liver Sinusoidal Endothelial Cell Fenestration and Protecting Against Hepatic Fibrosis
Desroches‐Castan, A., Tillet, E., Ricard, N., Ouarné, M., Mallet, C., Belmudes, L., Couté, Y., Boillot, O., Scoazec, J., Bailly, S., et al. (2019) · Hepatology · doi:10.1002/hep.30655 · Cited by 128 · see citing works
“”(27) These highly differentiated endothelial cells lose their characteristic fenestrae and display a marked decrease in their endocytic capacity.(30,41,45) This is accompanied by the production and release of paracrine factors as well as cellular microparticles and exosomes, which all affect the phenotype of neighbor…”
BackgroundResult
Liver fibrosis resolution: from molecular mechanisms to therapeutic opportunities
Pei, Q., Yi, Q., & Tang, L. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24119671 · Cited by 121 · see citing works
“Studies have demonstrated that LSECs can maintain HSCs quiescence through a vascular endothelial growth factor (VEGF)-stimulated pathway [42].”
Background
Angiocrine Wnt signaling controls liver growth and metabolic maturation in mice
Leibing, T., Géraud, C., Augustin, I., Boutros, M., Augustin, H. G., Okun, J. G., Langhans, C., Zierow, J., Wohlfeil, S. A., Olsavszky, V., et al. (2018) · Hepatology · doi:10.1002/hep.29613 · Cited by 116 · see citing works
“Dysfunctional HECs have been reported to be involved in metabolic and cirrhotic liver disease as well as cancer.((49,50)) Through altered LEIBING, G ERAUD, ET AL.”
Background
Hedgehog regulates yes‐associated protein 1 in regenerating mouse liver
Swiderska‐Syn, M., Xie, G., Michelotti, G. A., Jewell, M. L., Premont, R. T., Syn, W., & Diehl, A. M. (2016) · Hepatology · doi:10.1002/hep.28542 · Cited by 121 · see citing works
“Quiescent (Q)-HSCs are stimulated to become proliferative and myofibroblastic by various soluble factors that accumulate in injured livers,((1)) as well as injuryrelated alterations in liver blood flow((3)) and the physical characteristics of the liver matrix.”
Biology of portal hypertension
McConnell, M. J., & Iwakiri, Y. (2017) · Hepatology International · doi:10.1007/s12072-017-9826-x · Cited by 121 · see citing works
“The communication between LSECs and HSCs is important in the pathogenesis of portal hypertension, as evidenced by the fact that loss of LSEC phenotype can be permissive for HSC activation [40].”
Background
The roles and mechanisms of hypoxia in liver fibrosis
Cai, J., Hu, M., Chen, Z., & Ling, Z. (2021) · Journal of Translational Medicine · doi:10.1186/s12967-021-02854-x · Cited by 122 · see citing works
“ET-1 It is abundant in vascular smooth muscle cells, and its main task is to promote cell proliferation and mediate vascular contraction Promotes the HSC contraction and the secretion of cell matrix by HSC [27]”
Background
Functional Immune Anatomy of the Liver—As an Allograft
Demetris, A. J., Bellamy, C. O. C., Gandhi, C. R., Prost, S., Nakanuma, Y., & Stolz, D. B. (2016) · American Journal of Transplantation · doi:10.1111/ajt.13749 · Cited by 115 · see citing works
“3) Sinusoids are the majority microvasculature, lined by LSEC and KC (2, 5, 12, 16-19), which scavenge particulates/antigens, and regulate immune responses (2, 5, 12, 16-18, 20-22), liver regeneration(23-25), and fibrogenesis(25, 26).”
BackgroundInfluential
Portal Hypertension
Turco, L., & García–Tsao, G. (2019) · Clinics in Liver Disease · doi:10.1016/j.cld.2019.07.007 · Cited by 115 · see citing works
The Impact of Acute or Chronic Alcohol Intake on the NF-κB Signaling Pathway in Alcohol-Related Liver Disease
Nowak, A. J., & Relja, B. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21249407 · Cited by 107 · see citing works
“, the initial loss of liver endothelial cells fenestrae in ALD [67] that increases during chronic fibrosis and concludes in the strengthening of the LSECs defenestration effect [68].”
Background
Nanodrug with ROS and pH Dual‐Sensitivity Ameliorates Liver Fibrosis via Multicellular Regulation
Lin, L., Gong, H., Li, R., Huang, J., Cai, M., Lan, T., Huang, W., Guo, Y., Zhou, Z., An, Y., et al. (2020) · Advanced Science · doi:10.1002/advs.201903138 · Cited by 101 · see citing works
Five‐year histological and serological follow‐up of operationally tolerant pediatric liver transplant recipients enrolled in WISP‐R
Feng, S., Demetris, A. J., Spain, K. M., Kanaparthi, S., Burrell, B. E., Ekong, U. D., Alonso, E. M., Rosenthal, P. J., Turka, L. A., Iklé, D. N., et al. (2016) · Hepatology · doi:10.1002/hep.28681 · Cited by 101 · see citing works
“Whether undetectable arterial intimal LSEC injury or microvascular endothelial cell alterations (e.g., upregulation of complement regulatory proteins or cytoprotective molecules) are occurring is currently being investigated.”
Influential
Inhibition of canonical WNT signaling pathway by β-catenin/CBP inhibitor ICG-001 ameliorates liver fibrosis in vivo through suppression of stromal CXCL12
Akcora, B. Ö., Storm, G., & Bansal, R. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2017.12.001 · Cited by 98 · see citing works
“Furthermore, liver sinusoidal endothelial cells (LSECs) are required to maintain HSCs quiescence, and upon activation, partially via HSCs, become pro-inflammatory and therefore also play a critical role in intrahepatic inflammation [13-15].”
Background
Carvedilol as the new non‐selective beta‐blocker of choice in patients with cirrhosis and portal hypertension
Turco, L., Reiberger, T., Vitale, G., & Mura, V. L. (2023) · Liver International · doi:10.1111/liv.15559 · Cited by 98 · see citing works
Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells
(2025) · doi:10.1038/s41423-025-01313-7 · Cited by 97 · see citing works
Bergamot Polyphenols Improve Dyslipidemia and Pathophysiological Features in a Mouse Model of Non-Alcoholic Fatty Liver Disease
Musolino, V., Gliozzi, M., Scarano, F., Bosco, F., Scicchitano, M., Nucera, S., Carresi, C., Ruga, S., Zito, M. C., Maiuolo, J., et al. (2020) · Scientific Reports · doi:10.1038/s41598-020-59485-3 · Cited by 97 · see citing works
The wHole Story About Fenestrations in LSEC
Szafranska, K., Kruse, L. D., Holte, C. F., McCourt, P., & Zapotoczny, B. (2021) · Frontiers in Physiology · doi:10.3389/fphys.2021.735573 · Cited by 95 · see citing works
“Downregulation of VEGF signaling has been associated with LSEC defenestration, capillarization of sinusoids, and abnormal liver physiology (Carpenter et al., 2005; DeLeve, 2015).”
BackgroundInfluential
Macrophages evoke autophagy of hepatic stellate cells to promote liver fibrosis in NAFLD mice via the PGE2/EP4 pathway
Cao, Y., Mai, W., Li, R., Deng, S., Li, L.-J., Zhou, Y.-X., Qin, Q.-S., Zhang, Y., Zhou, X.-G., Han, M., et al. (2022) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-022-04319-w · Cited by 82 · see citing works
PPARs as Metabolic Sensors and Therapeutic Targets in Liver Diseases
Monroy-Ramírez, H. C., Galicia‐Moreno, M., Sandoval-Rodriguez, A. S., Meza-Ríos, A., Santos, A., & Armendáriz‐Borunda, J. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22158298 · Cited by 86 · see citing works
“Capillarization is a term used to describe when liver sinusoidal endothelial cells (LSECs) lack fenestration and develop an organized basement membrane, which is permissive for HSC activation and is a preamble to fibrosis [91].”
Background
The Human Amnion Epithelial Cell Secretome Decreases Hepatic Fibrosis in Mice with Chronic Liver Fibrosis
Alhomrani, M., Correia, J., Zavou, M. J., Leaw, B., Kuk, N., Xu, R., Saad, M. I., Hodge, A. D., Greening, D. W., Lim, R., et al. (2017) · Frontiers in Pharmacology · doi:10.3389/fphar.2017.00748 · Cited by 86 · see citing works
“However, CD206 is expressed in M2 liver macrophages as well as liver sinusoidal endothelial cells (DeLeve, 2015).”
Background
Liver Tropism in Cancer: The Hepatic Metastatic NichePreprint
Mielgo, A., & Schmid, M. C. (2019) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a037259 · Cited by 84 · see citing works
Angiocrine signaling in sinusoidal homeostasis and liver diseases
Gao, J., Lan, T., Kostallari, E., Guo, Y., Lai, E., Guillot, A., Ding, B., Tacke, F., Tang, C., & Shah, V. H. (2024) · Journal of Hepatology · doi:10.1016/j.jhep.2024.05.014 · Cited by 90 · see citing works
SECs (Sinusoidal Endothelial Cells), Liver Microenvironment, and Fibrosis
Natarajan, V., Harris, E. N., & Kidambi, S. (2017) · BioMed Research International · doi:10.1155/2017/4097205 · Cited by 84 · see citing works
“DeLeve and co-workers demonstrated that the capillarization of LSECs (loss in fenestrations) precedes the onset of fibrosis and acts as a gatekeeper event for the progression of liver fibrosis [30].”
Background
Pathological process of liver sinusoidal endothelial cells in liver diseases
Ni, Y., Li, J.-M., Liu, M., Zhang, T.-T., Wang, D., Zhou, W., Hu, L.-Z., & Lv, W. (2017) · World Journal of Gastroenterology · doi:10.3748/wjg.v23.i43.7666 · Cited by 83 · see citing works
High-dose systemic adeno-associated virus vector administration causes liver and sinusoidal endothelial cell injury
Hordeaux, J., Lamontagne, R. J., Song, C., Buchlis, G., Dyer, C., Buza, E. L., Ramezani, A., Wielechowski, E., Greig, J. A., Chichester, J. A., et al. (2024) · Molecular Therapy · doi:10.1016/j.ymthe.2024.02.002 · Cited by 81 · see citing works
Mechanotransduction in the pathogenesis of non-alcoholic fatty liver disease
Mitten, E. K., & Baffy, G. (2022) · Journal of Hepatology · doi:10.1016/j.jhep.2022.08.028 · Cited by 80 · see citing works
Sustained perfusion of revascularized bioengineered livers heterotopically transplanted into immunosuppressed pigs
Shaheen, M. F., Joo, D. J., Ross, J. J., Anderson, B. D., Chen, H. S., Huebert, R. C., Li, Y., Amiot, B., Young, A., Zlochiver, V., et al. (2019) · Nature Biomedical Engineering · doi:10.1038/s41551-019-0460-x · Cited by 75 · see citing works
Liver sinusoidal endothelial cell: An important yet often overlooked player in the liver fibrosis
Qu, J., Wang, L., Li, Y., & Li, X. (2024) · Clinical and Molecular Hepatology · doi:10.3350/cmh.2024.0022 · Cited by 74 · see citing works
“28 Meanwhile, LSECs can also stimulate neovascularization by secreting angiogenic factors, thereby fostering the fibrotic process.”
Background
Emerging therapeutic targets for the treatment of hepatic fibrosis
Fagone, P., Mangano, K., Pesce, A., Portale, T. R., Puleo, S., & Nicoletti, F. (2015) · Drug Discovery Today · doi:10.1016/j.drudis.2015.10.015 · Cited by 75 · see citing works
Sphingosine‐1‐phosphate promotes tumor development and liver fibrosis in mouse model of congestive hepatopathy
Kawai, H., Osawa, Y., Matsuda, M., Tsunoda, T., Yanagida, K., Hishikawa, D., Okawara, M., Sakamoto, Y., Shimagaki, T., Tsutsui, Y., et al. (2022) · Hepatology · doi:10.1002/hep.32256 · Cited by 72 · see citing works
Liver sinusoidal endothelial cell expressed vascular cell adhesion molecule 1 promotes liver fibrosis
Guo, Q., Furuta, K., Islam, S., Caporarello, N., Kostallari, E., Dielis, K., Tschumperlin, D. J., Hirsova, P., & Ibrahim, S. H. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.983255 · Cited by 73 · see citing works
“Differentiated LSECs (LSECs under physiological conditions) can maintain HSC quiescence in a paracrine manner (7, 25).”
BackgroundInfluential
Genome-wide analysis of DNA methylation and gene expression patterns in purified, uncultured human liver cells and activated hepatic stellate cells
Taghdouini, A. E., Sørensen, A. L., Reiner, A. H., Coll, M., Verhulst, S., Mannaerts, I., Øie, C. I., Smedsrød, B. H., Najimi, M., Sokal, E. M., et al. (2015) · Oncotarget · doi:10.18632/oncotarget.4925 · Cited by 72 · see citing works
“These pathologies are characterized by impairment of hepatocyte (HEP) function [3], liver sinusoidal endothelial cell (LSEC) capillarization [4] and activation of hepatic stellate cells (HSCs) and Kupffer cells (KCs) [5, 6].”
Background
Towards improved hepatocyte cultures: Progress and limitations
Ruoß, M., Vosough, M., Königsrainer, A., Nadalin, S., Wagner, S., Sajadian, S., Huber, D., Heydari, Z., Ehnert, S., Hengstler, J. G., et al. (2020) · Food and Chemical Toxicology · doi:10.1016/j.fct.2020.111188 · Cited by 77 · see citing works
Liver fibrosis in biliary atresia
Shen, W.-J., Chen, G., Wang, M., & Zheng, S. (2018) · World Journal of Pediatrics · doi:10.1007/s12519-018-0203-1 · Cited by 72 · see citing works
Angiocrine signaling in the hepatic sinusoids in health and disease
Kostallari, E., & Shah, V. H. (2016) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00118.2016 · Cited by 71 · see citing works
Liver Microvascular Injury and Thrombocytopenia of Antibody–Calicheamicin Conjugates in Cynomolgus Monkeys—Mechanism and Monitoring
Guffroy, M., Falahatpisheh, H., Biddle, K. E., Kreeger, J., Obert, L., Walters, K. M., Goldstein, R., Boucher, G., Coskran, T., Reagan, W. J., et al. (2016) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-16-0939 · Cited by 70 · see citing works
“, development of a basement membrane and loss of fenestrations) and liver functional impairment (17, 35).”
Background
Capillarized Liver Sinusoidal Endothelial Cells Undergo Partial Endothelial-Mesenchymal Transition to Actively Deposit Sinusoidal ECM in Liver Fibrosis
Ruan, B., Duan, J., Xu, H., Tao, K., Han, H., Dou, G., & Wang, L. (2021) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.671081 · Cited by 72 · see citing works
“It is wellknown that LSECs undergo capillarization in fibrosis (DeLeve, 2015; Marrone et al., 2016; Poisson et al., 2017).”
Background
Overlooked subclinical portal hypertension in non-cirrhotic NAFLD: Is it real and how to measure it?
Baffy, G., & Bosch, J. (2021) · Journal of Hepatology · doi:10.1016/j.jhep.2021.09.029 · Cited by 69 · see citing works
Oroxylin A prevents angiogenesis of LSECs in liver fibrosis via inhibition of YAP/HIF‐1α signaling
Zhang, C., Bian, M., Chen, X., Jin, H., Zhao, S., Xiang, Y., Shao, J., Chen, A., Guo, Q., Zhang, F., et al. (2017) · Journal of Cellular Biochemistry · doi:10.1002/jcb.26388 · Cited by 69 · see citing works
Intercellular Communication between Hepatic Cells in Liver Diseases
Sato, K., Kennedy, L. L., Liangpunsakul, S., Kusumanchi, P., Yang, Z., Meng, F., Glaser, S. S., Francis, H., & Alpini, G. D. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20092180 · Cited by 68 · see citing works
“LSECs are located near HSCs (Figure 1), and crosstalk between LSECs and HSCs is associated with liver fibrosis [49].”
Background
Prevention of hepatic stellate cell activation using JQ1- and atorvastatin-loaded chitosan nanoparticles as a promising approach in therapy of liver fibrosis
Hassan, R., Tammam, S. N., Elsafy, S., Abdel‐Halim, M., Asimakopoulou, A., Weiskirchen, R., & Mansour, S. (2018) · European Journal of Pharmaceutics and Biopharmaceutics · doi:10.1016/j.ejpb.2018.11.018 · Cited by 66 · see citing works
Neuropilin-1 aggravates liver cirrhosis by promoting angiogenesis via VEGFR2-dependent PI3K/Akt pathway in hepatic sinusoidal endothelial cells
Wang, L., Feng, Y., Xie, X., Wu, H., Su, X. N., Qi, J., Xin, W., Gao, L., Zhang, Y., Shah, V. H., et al. (2019) · EBioMedicine · doi:10.1016/j.ebiom.2019.04.050 · Cited by 66 · see citing works
“HSECs represent the highest proportion of non-parenchymal cells in the liver and are alsomajor co-modulators offibrogenesis in addition toHSCs [3].”
Background
In Vitro Models for the Study of Liver Biology and Diseases: Advances and Limitations
Kaur, S., Kidambi, S., Ortega‐Ribera, M., Thủy, L. T. T., Nieto, N., Cogger, V. C., Xie, W., Tacke, F., & Gracia‐Sancho, J. (2022) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2022.11.008 · Cited by 67 · see citing works
The liver fibrosis niche: Novel insights into the interplay between fibrosis-composing mesenchymal cells, immune cells, endothelial cells, and extracellular matrix
Matsuda, M., & Seki, E. (2020) · Food and Chemical Toxicology · doi:10.1016/j.fct.2020.111556 · Cited by 64 · see citing works
Mechanosensing in liver regeneration
Song, Z., Gupta, K., Ng, I. C., Xing, J., Yang, Y. A., & Yu, H. (2017) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2017.07.041 · Cited by 63 · see citing works
Carvedilol attenuates carbon tetrachloride-induced liver fibrosis and hepatic sinusoidal capillarization in mice
Wu, Y., Li, Z., Xiu, A., Meng, D., Wang, S.-N., & Zhang, C. (2019) · Drug Design Development and Therapy · doi:10.2147/dddt.s210797 · Cited by 63 · see citing works
“38,39 It has been reported that LSEC capillarization promotes HSC activation and ﬁ brosis and the reversal of LSEC capillarization could promote the quiescence of HSCs. 40 The interaction between LSECs and HSCs increases collagen deposition, promotes ﬁ brogenesis and angiogenesis.”
Background
Liver, ageing and disease
Couteur, D. G. L., Ngu, M., Hunt, N. J., Brandon, A. E., Simpson, S. J., & Cogger, V. C. (2025) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-025-01099-z · Cited by 64 · see citing works
“Age-related LSEC defenestration and dysfunction are critical steps in the progression of the ageing liver to a steatotic and fibrotic liver 118,120 .”
New Concepts on Pathogenesis and Diagnosis of Liver Fibrosis; A Review Article
Ebrahimi, H., Naderian, M., & Sohrabpour, A. A. (2016) · Middle East Journal of Digestive Diseases · doi:10.15171/mejdd.2016.29 · Cited by 61 · see citing works
Hepatic Endothelial Notch Activation Protects against Liver Metastasis by Regulating Endothelial-Tumor Cell Adhesion Independent of Angiocrine Signaling
Wohlfeil, S. A., Häfele, V., Dietsch, B., Schledzewski, K., Winkler, M., Zierow, J., Leibing, T., Mohammadi, M. M., Heineke, J., Sticht, C., et al. (2018) · Cancer Research · doi:10.1158/0008-5472.can-18-1752 · Cited by 62 · see citing works
“Sinusoidal capillarization is regularly observed in fibrotic/cirrhotic liver diseases (42) associated with fewer liver metastases.”
Background
Liver endothelial cells in NAFLD and transition to NASH and HCC
Velliou, R.-I., Legaki, A., Nikolakopoulou, P., Vlachogiannis, N. I., & Chatzigeorgiou, A. (2023) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-04966-7 · Cited by 63 · see citing works
ABO-compatible liver allograft antibody-mediated rejection
Demetris, A. J., Zeevi, A., & O’Leary, J. G. (2015) · Current Opinion in Organ Transplantation · doi:10.1097/mot.0000000000000194 · Cited by 61 · see citing works
“Fourth, liver sinusoidal endothelial cells express Fc receptors [48] and lack a typical basement membrane: they are also normally”
Role of liver sinusoidal endothelial cell in metabolic dysfunction-associated fatty liver disease
He, Q., He, W., Dong, H., Guo, Y., Yuan, G., Shi, X., Wang, D., & Lu, F. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-024-01720-9 · Cited by 61 · see citing works
“In vitro studies have shown that differentiated LSECs can prevent HSCs activation and promote the return of activated HSC (aHSC) to quiet HSC (qHSC) through VEGF-A-stimulated NO production, but LSECs will lose this effect during dedif-ferentiation or capillarization [65, 83],”
Background
Alcoholic Liver Disease: Current Mechanistic Aspects with Focus on Their Clinical Relevance
Teschke, R. (2019) · Biomedicines · doi:10.3390/biomedicines7030068 · Cited by 61 · see citing works
Restoration of Sinusoid Fenestrae Followed by Targeted Nanoassembly Delivery of an Anti‐Fibrotic Agent Improves Treatment Efficacy in Liver Fibrosis
Li, F., Zhao, Y., Cheng, Z., Wang, Y., Yue, Y., Cheng, X., Sun, J., Atabakhshi‐Kashi, M., Yao, J., Dou, J., et al. (2023) · Advanced Materials · doi:10.1002/adma.202212206 · Cited by 59 · see citing works
Tyrosine kinase inhibitor BIBF1120 ameliorates inflammation, angiogenesis and fibrosis in CCl4-induced liver fibrogenesis mouse model
Akcora, B. Ö., Storm, G., Prakash, J., & Bansal, R. (2017) · Scientific Reports · doi:10.1038/srep44545 · Cited by 59 · see citing works
“Liver sinusoidal endothelial cells (LSECs) has shown to play a critical role in liver fibrosis 17,18 .”
New aspects of hepatic endothelial cells in physiology and nonalcoholic fatty liver disease
Sun, X., & Harris, E. N. (2020) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00062.2020 · Cited by 58 · see citing works
Contributions of Fibroblasts, Extracellular Matrix, Stiffness, and Mechanosensing to Hepatocarcinogenesis
Filliol, A. A., & Schwabe, R. F. (2019) · Seminars in Liver Disease · doi:10.1055/s-0039-1685539 · Cited by 58 · see citing works
Manipulating fenestrations in young and old liver sinusoidal endothelial cells
Hunt, N. J., Lockwood, G. P., Warren, A., Mao, H., McCourt, P., Couteur, D. G. L., & Cogger, V. C. (2018) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00179.2018 · Cited by 58 · see citing works
“The regulation of LSEC fenestrations has been recently reviewed, and the major regulatory pathway is thought to be mediated by VEGF and NO (16).”
Background
Liver sinusoidal endothelial cells (LSECs) modifications in patients with chronic hepatitis C
Baiocchini, A., Nonno, F. D., Taibi, C., Comandini, U. V., D’Offizi, G., Piacentini, M., & Falasca, L. (2019) · Scientific Reports · doi:10.1038/s41598-019-45114-1 · Cited by 58 · see citing works
Endothelial Dysfunction in Pathological Processes of Chronic Liver Disease during Aging
Wan, Y., Li, X., Slevin, E., Harrison, K., Li, T., Zhang, Y.-D., Klaunig, J., Wu, C.-D., Shetty, A. K., Dong, X. C., et al. (2021) · The FASEB Journal · doi:10.1096/fj.202101426r · Cited by 55 · see citing works
LncRNA Airn maintains LSEC differentiation to alleviate liver fibrosis via the KLF2-eNOS-sGC pathway
Chen, T., Shi, Z., Zhao, Y., Meng, X., Zhao, S., Zheng, L., Han, X., Hu, Z., Yao, Q., Lin, H., et al. (2022) · BMC Medicine · doi:10.1186/s12916-022-02523-w · Cited by 57 · see citing works
“Capillarized LSEC have been shown to precede fibrosis and promote HSC activation and hepatocyte damage [8].”
BackgroundInfluential
The role of liver sinusoidal endothelial cells in cancer liver metastasis.
Yang, M. J., & Zhang, C. (2021) · PubMed Central · Cited by 56 · see citing works

Role of Differentiation of Liver Sinusoidal Endothelial Cells in Progression and Regression of Hepatic Fibrosis in Rats
Xie, G., Wang, X., Wang, L., Wang, L., Atkinson, R. D., Kanel, G. C., Gaarde, W. A., & DeLeve, L. D. (2012) · Gastroenterology · doi:10.1053/j.gastro.2011.12.017 · Cited by 410 · see citing works
Self-citation
Liver sinusoidal endothelial cells in disease – And for therapy?
Stutchfield, B. M., & Forbes, S. J. (2012) · Journal of Hepatology · doi:10.1016/j.jhep.2012.07.046 · Cited by 9 · see citing works
Sinusoidal endothelial cell crosstalk with other liver cells
DeLeve, L. D., & Wang, X. (2009) · The FASEB Journal · doi:10.1096/fasebj.23.1_supplement.66.2
Self-citation
Key role of liver sinusoidal endothelial cells in liver fibrosis.
Xu, M.-X., Wang, X.-H., Zou, Y., & Zhong, Y.-S. (2017) · BioScience Trends · doi:10.5582/bst.2017.01007 · Cited by 38 · see citing works
Incomplete Differentiation of Engrafted Bone Marrow Endothelial Progenitor Cells Initiates Hepatic Fibrosis in the Rat
Maretti-Mira, A. C., Wang, X., Wang, L., & DeLeve, L. D. (2018) · Hepatology · doi:10.1002/hep.30227 · Cited by 49 · see citing works
Self-citation

Authors: DeLeve, L. D.
Affiliations: University of Southern California (US)
Corresponding author: DeLeve, Laurie D.
ORCID: DeLeve, Laurie D.
Venue: Hepatology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2015-03-23
Volume: 61
Issue: 5
Pages: 1740-1746
ISSN: 0270-9139 (ISSN-L)
1527-3350
DOI: 10.1002/hep.27376
PMC: PMC4333127
OpenAlex: W1781806439
Cited by: 482
References: 50
Citations by year: 2026: 45 · 2025: 44 · 2024: 60 · 2023: 40 · 2022: 39 · 2021: 51 · 2020: 49 · 2019: 37 · 2018: 46 · 2017: 35 · 2016: 26 · 2015: 9 · 2014: 1
FWCI: 3.08
Type: journal article
Language: en
Update notices: correction (2015-07-01)
Open access: green
www.ncbi.nlm.nih.gov
Licence: doi.wiley.com/10.1002/tdm_license_1.1 (tdm, 162 d)
Locations: Hepatology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK100580, DK-66423, R01DK066423)
Topics: Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
Keywords: liver sinusoidal endothelial cells, liver fibrosis, capillarization, endothelial fenestrations, basement membrane formation, hepatic stellate cell activation, VEGF signaling, nitric oxide, HSC quiescence, fibrosis regression, liver cirrhosis
MeSH terms: Cell Differentiation, Humans, Liver Cirrhosis, Endothelial Cells

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

Liver sinusoidal endothelial cells in hepatic fibrosis

Abstract

Integrity signals

Claims the paper makes

Claims other papers make about this one

Self-check

Cites

Cited by

Related

Record

About these checks