ArticleFrontiers in physiology2019
LSEC Fenestrae Are Preserved Despite Pro-inflammatory Phenotype of Liver Sinusoidal Endothelial Cells in Mice on High Fat Diet.
Article in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 63 citations in OpenAlex.
- Liver sinusoidal endothelial cell defenestration in chronic heart failure is primarily dependent on cardiac diastolic dysfunction and is reversed by a sodium-glucose cotransporter 2 inhibitor but not by an angiotensin-converting enzyme inhibitor.Cardiovascular research · 2026Article
- Liver sinusoidal endothelial cell fenestrations in metabolic liver disease: from molecular mechanisms to therapeutic perspectives.Cell communication and signaling : CCS · 2026Review
- Metabolic Pathways Linking Atherosclerotic Cardiovascular Disease With Metabolic Dysfunction-Associated Steatotic Liver Disease.Current atherosclerosis reports · 2026Review
- Metabolic adaptations in cancer progression.Physiological reviews · 2026Review
- Liver, ageing and disease.Nature reviews. Gastroenterology & hepatology · 2025Review
- Loss of endothelial ZEB2 in mice attenuates steatosis early during metabolic dysfunction-associated steatotic liver disease.Scientific reports · 2025Article
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- Aging and metabolic dysfunction-associated steatotic liver disease: a bidirectional relationship.Frontiers of medicine · 2025Review
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- The role of liver sinusoidal endothelial cells in metabolic dysfunction-associated steatotic liver diseases and liver cancer: mechanisms and potential therapies.Angiogenesis · 2025Review
- The role of hepatic sinusoidal microenvironment in NASH: pathogenesis, animal models, and therapeutic prospects.Frontiers in pharmacology · 2025Review
- Early and late phases of liver sinusoidal endothelial cell (LSEC) defenestration in mouse model of systemic inflammation.Cellular & molecular biology letters · 2024Article
- Protein disulfide isomerase A1 regulates fenestration dynamics in primary mouse liver sinusoidal endothelial cells (LSECs).Redox biology · 2024Article
- Liver sinusoidal endothelial cells rely on oxidative phosphorylation but avoid processing long-chain fatty acids in their mitochondria.Cellular & molecular biology letters · 2024Article
- Dynamic YAP expression in the non-parenchymal liver cell compartment controls heterologous cell communication.Cellular and molecular life sciences : CMLS · 2024Article
- Endothelial Slc35a1 Deficiency Causes Loss of LSEC Identity and Exacerbates Neonatal Lipid Deposition in the Liver in Mice.Cellular and molecular gastroenterology and hepatology · 2024Article
- Mouse liver sinusoidal endothelial cell responses to the glucocorticoid receptor agonist dexamethasone.Frontiers in pharmacology · 2024Article
- Angiocrine Signaling in Sinusoidal Health and Disease.Seminars in liver disease · 2023Review
- Age-related liver endothelial zonation triggers steatohepatitis by inactivating pericentral endothelium-derived C-kit.Nature aging · 2023Article
- [Research progress of liver sinusoidal endothelial cells in nonalcoholic fatty liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023Review
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Healthy liver sinusoidal endothelial cells (LSECs) maintain liver homeostasis, while LSEC dysfunction was suggested to coincide with defenestration. Here, we have revisited the relationship between LSEC pro-inflammatory response, defenestration, and impairment of LSEC bioenergetics in non-alcoholic fatty liver disease (NAFLD) in mice. We characterized inflammatory response, morphology as well as bioenergetics of LSECs in early and late phases of high fat diet (HFD)-induced NAFLD. LSEC phenotype was evaluated at early (2-8 week) and late (15-20 week) stages of NAFLD progression induced by HFD in male C57Bl/6 mice. NAFLD progression was monitored by insulin resistance, liver steatosis and obesity. LSEC phenotype was determined in isolated, primary LSECs by immunocytochemistry, mRNA gene expression (qRT-PCR), secreted prostanoids (LC/MS/MS) and bioenergetics (Seahorse FX Analyzer). LSEC morphology was examined using SEM and AFM techniques. Early phase of NAFLD, characterized by significant liver steatosis and prominent insulin resistance, was related with LSEC pro-inflammatory phenotype as evidenced by elevated ICAM-1, E-selectin and PECAM-1 expression. Transiently impaired mitochondrial phosphorylation in LSECs was compensated by increased glycolysis. Late stage of NAFLD was featured by prominent activation of pro-inflammatory LSEC phenotype (ICAM-1, E-selectin, PECAM-1 expression, increased COX-2, IL-6, and NOX-2 mRNA expression), activation of pro-inflammatory prostaglandins release (PGE
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