The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
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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Cites
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…”
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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
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
“This distribution could be related to the progressive decrease in oxygen tension along the lobule accompanied with an increasing need for oxygen exchange [36].”
BackgroundAngiocrine functions of organ-specific endothelial cells
Rafii, S., Butler, J. M., & Ding, B. (2016) · Nature · doi:10.1038/nature17040 · Cited by 963
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 911
Organotypic vasculature: From descriptive heterogeneity to functional pathophysiology
Augustin, H. G., & Koh, G. Y. (2017) · Science · doi:10.1126/science.aal2379 · Cited by 790
“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
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
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