New aspects of hepatic endothelial cells in physiology and nonalcoholic fatty liver disease.
Animals
Autophagy
Capillaries
/ metabolism
Cell Differentiation
Cell Proliferation
Cellular Senescence
Endothelial Cells
/ metabolism
Epithelial-Mesenchymal Transition
Humans
Inflammation Mediators
/ metabolism
Liver
/ blood supply
Liver Cirrhosis
/ metabolism
Mechanotransduction, Cellular
Non-alcoholic Fatty Liver Disease
/ metabolism
Paracrine Communication
Reactive Oxygen Species
/ metabolism
LSECs
NAFLD
autophagy
cellular senescence
fibrosis
hepatic endothelium
scavenger function
Journal
American journal of physiology. Cell physiology
ISSN: 1522-1563
Titre abrégé: Am J Physiol Cell Physiol
Pays: United States
ID NLM: 100901225
Informations de publication
Date de publication:
01 06 2020
01 06 2020
Historique:
pubmed:
7
5
2020
medline:
4
8
2020
entrez:
7
5
2020
Statut:
ppublish
Résumé
The liver is the central metabolic hub for carbohydrate, lipid, and protein metabolism. It is composed of four major types of cells, including hepatocytes, endothelial cells (ECs), Kupffer cells, and stellate cells. Hepatic ECs are highly heterogeneous in both mice and humans, representing the second largest population of cells in liver. The majority of them line hepatic sinusoids known as liver sinusoidal ECs (LSECs). The structure and biology of LSECs and their roles in physiology and liver disease were reviewed recently. Here, we do not give a comprehensive review of LSEC structure, function, or pathophysiology. Instead, we focus on the recent progress in LSEC research and other hepatic ECs in physiology and nonalcoholic fatty liver disease and other hepatic fibrosis-related conditions. We discuss several current areas of interest, including capillarization, scavenger function, autophagy, cellular senescence, paracrine effects, and mechanotransduction. In addition, we summarize the strengths and weaknesses of evidence for the potential role of endothelial-to-mesenchymal transition in liver fibrosis.
Identifiants
pubmed: 32374676
doi: 10.1152/ajpcell.00062.2020
pmc: PMC7311747
doi:
Substances chimiques
Inflammation Mediators
0
Reactive Oxygen Species
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
C1200-C1213Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM104320
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL130864
Pays : United States
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