The evolving role of liver sinusoidal endothelial cells in liver health and disease
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LSECs are a unique population of endothelial cells within the liver and are recognized as key regulators of liver homeostasis. LSECs also play a key role in liver disease, as dysregulation of their quiescent phenotype promotes pathological processes within the liver including inflammation, microvascular thrombosis, fibrosis, and portal hypertension. Recent technical advances in single-cell analysis have characterized distinct subpopulations of the LSECs themselves with a high resolution and defined their gene expression profile and phenotype, broadening our understanding of their mechanistic role in liver biology. This article will review 4 broad advances in our understanding of LSEC biology in general: (1) LSEC heterogeneity, (2) LSEC aging and senescence, (3) LSEC role in liver regeneration, and (4) LSEC role in liver inflammation and will then review the role of LSECs in various liver pathologies including fibrosis, DILI, alcohol-associated liver disease, NASH, viral hepatitis, liver transplant rejection, and ischemia reperfusion injury. The review will conclude with a discussion of gaps in knowledge and areas for future research.
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In the adult liver, endothelial cells appear to be zonated. scRNA-seq revealed that periportal LSECs express high levels of CD36 and Adam23, which progressively diminish in the midzonal and pericentral zones. On the other hand, pericentral LSECs and central venous ECs abundantly express Wnt2, Wnt9, Lhx6, and Kit, which decrease toward midzonal and periportal zone ECs. Flt4, Lyve1, Cd32b, and Stab
“In the adult liver, endothelial cells appear to be zonated. scRNA-seq revealed that periportal LSECs express high levels of CD36 and Adam23, which progressively diminish in the midzonal and pericentral zones. On the other hand, pericentral LSECs and central venous ECs abundantly express Wnt2, Wnt9, Lhx6, and Kit, which decrease toward midzonal and periportal zone ECs. Flt4, Lyve1, Cd32b, and Stab”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [292]
Alcoholic hepatitis is the most severe manifestation of alcohol-associated liver disease and presents an accumulation of neutrophils in the liver.
“Alcoholic hepatitis (AH) is the most severe manifestation of ALD and presents an accumulation of neutrophils in the liver [292, 311].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [292]
The proinflammatory phenotype of LSECs in MASLD and MASH is characterized by loss of fenestrae and increased expression of adhesion molecules.
“The proinflammatory phenotype of LSECs has also been explored in MASLD and MASH, where they are characterized by a loss of fenestrae and increased expression of adhesion molecules [292].”
From Inflammation and immunity in liver homeostasis and disease: a nexus of hepatocytes, nonparenchymal cells and immune cells (2025) · cites this paper as [292]
Alcohol metabolism reduces the NAD+/NADH ratio and impairs mitochondrial fatty acid oxidation, which can induce hepatic steatosis.
“Alcohol metabolism also reduces the NAD+/NADH ratio and impairs mitochondrial fatty acid oxidation, which can induce hepatic steatosis [100, 101].”
From Constructing biomimetic microenvironments for liver regeneration (2025) · cites this paper as [100]
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Self-citation
- Authors
- McConnell, M. J., Kostallari, E., Ibrahim, S. H., & Iwakiri, Y.
- Affiliations
- Yale University (US)
- Mayo Clinic (US)
- Corresponding author
- Ibrahim, Samar H.
- Iwakiri, Yasuko
- Venue
- Hepatology
- Published
- 2023-01-03
- Volume
- 78
- Issue
- 2
- Pages
- 649-669
- ISSN
- 0270-9139 (ISSN-L)
- PMC
- PMC10315420
- OpenAlex
- W4315619819
- Cited by
- 189
- References
- 194
- Citations by year
- 2026: 76 · 2025: 65 · 2024: 37 · 2023: 11
- FWCI
- 8.16
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Gilead Sciences
- Regenerative Medicine Minnesota
- National Institutes of Health
- Center for Cell Signaling in Gastroenterology, Mayo Clinic
- National Institute on Alcohol Abuse and Alcoholism (R01AA025342, K08AA029182)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK117597, R01DK130362, R01DK121511, P30DK034989, P30DK084567, R01DK122948)
- Yale Center for Clinical Investigation, Yale School of Medicine
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Hepatology › Liver Disease and Transplantation
- Health Sciences › Medicine › Surgery › Organ Transplantation Techniques and Outcomes
- Keywords
- liver sinusoidal endothelial cells, liver regeneration, liver inflammation, liver fibrosis, drug-induced liver injury, alcoholic liver disease, nonalcoholic steatohepatitis, viral hepatitis, liver transplant rejection, ischemia-reperfusion injury, portal hypertension, microvascular thrombosis, liver homeostasis
- MeSH terms
- Fibrosis, Humans, Inflammation, Liver, Liver Diseases, Endothelial Cells
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