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Liver sinusoidal endothelial cells in hepatic fibrosis
Open accessAbstract
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)
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“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]
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“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]
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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×
“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.”
BackgroundLimmer, 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×
“In normal liver, LSECs are tolerogenic (44, 45).”
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×
“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×
“INTRODUCTION Capillarization, which is when liver sinusoidal endothelial cells (LSECs) lack fenestration and develop an organized basement membrane (1), is a prelude to fibrosis.”
Corpechot, C., Barbu, V., Wendum, D., Kinnman, N., Rey, C., Poupon, R. Y., Housset, C., & Rosmorduc, O. (2002) · Hepatology · doi:10.1053/jhep.2002.32524 · Cited by 483 · cited 1×
“VEGF is upregulated in cirrhosis (33, 34), so that total VEGF is not rate limiting in this process.”
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×
“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.”
BackgroundCarreira, C. M., Nasser, S. M., di Tomaso, E., Padera, T. P., Boucher, Y., Tomarev, S. I., & Jain, R. K. (2001) · PubMed · Cited by 444
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×
“During resolution of fibrosis, the decline in activated HSC is due to both reversion to quiescence and apoptosis (28, 50).”
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
Self-citationDeLeve, L. D., Wang, X., & Guo, Y. (2008) · Hepatology · doi:10.1002/hep.22351 · Cited by 408 · cited 5×
“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-citationRockey, D. C., & Chung, J. J. (1998) · Gastroenterology · doi:10.1016/s0016-5085(98)70487-1 · Cited by 408 · cited 2×
“In cirrhosis, decreased production of NO by LSECs (31) and increased production of endothelin-1 by HSCs promotes contractility of HSCs (38) and”
Nagelkerke, J. F., Barto, K. P., & van Berkel, T. J. C. (1983) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)44160-3 · Cited by 386 · cited 1×
“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…”
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×
“SIGN; aka CD209L or DC-SIGN-related (DC SIGNR)] (19), and LYVE-1 (20, 21).”
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×
“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.”
BackgroundStabilin-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
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 307 · cited 1×
“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…”
BackgroundKNOLLE, 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×
“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
Self-citationvan Berkel, T. J. C., de Rijke, Y. B., & Kruijt, J. K. (1991) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(18)52241-9 · Cited by 277 · cited 1×
“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…”
Yamane, A., Seetharam, L., Yamaguchi, S., Gotoh, N., Takahashi, T., Neufeld, G., & Shibuya, M. (1994) · PubMed · Cited by 251
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×
“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.”
BackgroundMarrone, 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×
“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…”
BackgroundThe 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
Smedsrød, B. H., Melkko, J., Araki, N., Sano, H., & Horiuchi, S. (1997) · Biochemical Journal · doi:10.1042/bj3220567 · Cited by 224 · cited 1×
“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…”
BackgroundStabilin-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×
“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 182 · cited 1×
“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×
“FcγIIb2 (CD32b or SE-1 (16)), clears immune complexes formed with Ig G (17).”
McCourt, P., Smedsrød, B. H., Melkko, J., & Johansson, S. (1999) · Hepatology · doi:10.1002/hep.510300521 · Cited by 144 · cited 1×
“The hyaluronan/scavenger receptor, SR-H (stabilin-1 and stabilin-2), is the main functional scavenger receptor on the LSEC (6-8).”
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
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×
“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 135 · cited 1×
“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.”
BackgroundBlomhoff, 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×
“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…”
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×
“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.”
BackgroundMalovic, 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×
“, 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…”
BackgroundIn 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. L., Cohen, S., et al. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.1000332 · Cited by 120 · cited 1×
“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.”
BackgroundMartens, 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
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
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
Self-citationMousavi, S. A., Sporstφl, M., Fladeby, C., Kjeken, R., Barois, N., & Berg, T. (2007) · Hepatology · doi:10.1002/hep.21748 · Cited by 113 · cited 2×
“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×
“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…”
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×
“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.”
BackgroundKnorr, 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×
“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×
“In cirrhosis, decreased production of NO by LSECs (31) and increased production of endothelin-1 by HSCs promotes contractility of HSCs (38) and”
Nonaka, H., Tanaka, M., Suzuki, K., & Miyajima, A. (2007) · Developmental Dynamics · doi:10.1002/dvdy.21227 · Cited by 84 · cited 2×
“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.”
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 78 · cited 1×
“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-citationTamaki, S., Ueno, T., Torimura, T., Sata, M., & Tanikawa, K. (1996) · Gastroenterology · doi:10.1016/s0016-5085(96)70074-4 · Cited by 75 · cited 1×
“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.”
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×
“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…”
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×
“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…”
BackgroundOlsen, 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 50 · cited 2×
“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…”
BackgroundEskild, 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×
“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…”
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×
“VEGF is upregulated in cirrhosis (33, 34), so that total VEGF is not rate limiting in this process.”
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Background
Metadata
- Authors
- DeLeve, L. D.
- Affiliations
- University of Southern California (US)
- Corresponding author
- DeLeve, Laurie D.
- ORCID
- DeLeve, Laurie D.
- Venue
- Hepatology
- Published
- 2015-03-23
- Volume
- 61
- Issue
- 5
- Pages
- 1740-1746
- ISSN
- 0270-9139 (ISSN-L)
- 1527-3350
- 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
- FWCI
- 3.08
- Type
- journal article
- Language
- en
- Update notices
- correction (2015-07-01)
- Open access
- green
- www.ncbi.nlm.nih.gov
- 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 › Hepatology › 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 ›
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