ArticleCell death & disease2018
Autophagic degradation of caveolin-1 promotes liver sinusoidal endothelial cells defenestration.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 50 citations in OpenAlex.
- Dietary, Nutrient, and Supramolecular Nanofiber Modulation of the Liver Sinusoidal Clearance System in Metabolic Diseases and Aging.Biomedicines · 2026Review
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- Mechanical mechanics-reclaiming a new battlefield for chronic liver disease.Journal of advanced research · 2026Review
- Ferroptosis nanomedicine for cancer therapy: strategies and challenges.Frontiers in molecular biosciences · 2026Review
- Effects of curcumol on ferroptosis and tube forming ability of hepatic sinus endothelial cells.Open medicine (Warsaw, Poland) · 2026Article
- Cell-specific roles of autophagy in liver fibrosis: implications for targeted pharmacotherapy.Annals of medicine · 2025Review
- CASC15 participated in the damage of vascular endothelial cells in atherosclerosis through interaction with miR-940.BMC medical genomics · 2025Article
- Liver sinusoidal endothelial cell: An important yet often overlooked player in the liver fibrosis.Clinical and molecular hepatology · 2024Review
- Autophagy in hepatic progenitor cells modulates exosomal miRNAs to inhibit liver fibrosis in schistosomiasis.Frontiers of medicine · 2024Article
- Article
- Autophagic degradation of MVBs in LSECs promotes Aldosterone induced-HSCs activation.Hepatology international · 2024Article
- Dysfunction of autophagy in high-fat diet-induced non-alcoholic fatty liver disease.Autophagy · 2024Review
- The unique structural and functional characteristics of glomerular endothelial cell fenestrations and their potential as a therapeutic target in kidney disease.American journal of physiology. Renal physiology · 2023Review
- Cortisol Rapidly Facilitates Glucocorticoid Receptor Translocation to the Plasma Membrane in Primary Trout Hepatocytes.Biology · 2023Article
- Article
- Caveolin-1 influences mitochondrial plasticity and function in hepatic stellate cell activation.Cell biology international · 2022Article
- Review
- Prevention of D-GalN/LPS-induced ALI by 18β-glycyrrhetinic acid through PXR-mediated inhibition of autophagy degradation.Cell death & disease · 2021Article
- Sirtuin 1 ameliorates defenestration in hepatic sinusoidal endothelial cells during liver fibrosis via inhibiting stress-induced premature senescence.Cell proliferation · 2021Article
- Autophagy in liver diseases.World journal of hepatology · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy, interacting with actin cytoskeleton and the NO-dependent pathway, may affect the phenotype and function of endothelial cells. Moreover, caveolin-1 (Cav-1), as a structure protein in liver sinusoidal endothelial cells (LSECs), is closely related to autophagy. Hence, we aim to explore the role of autophagic degradation of Cav-1 in LSECs defenestration. In vivo, we found the increase of autophagy in liver sinusoidal endothelium in human fibrotic liver. Furthermore, autophagy, degradation of Cav-1, and actin filament (F-actin) remodeling were triggered during the process of CCl4-induced LSECs defenestration; in contrast, autophagy inhibitor 3MA diminished the degradation of Cav-1 to maintain fenestrae and relieve CCl4-induced fibrosis. In vitro, during LSECs defenestration, the NO-dependent pathway was down-regulated through the reduction of the PI3K-AKT-MTOR pathway and initiation of autophagic degradation of Cav-1; while, these effects were aggravated by starvation. However, VEGF inhibited autophagic degradation of Cav-1 and F-actin remodeling to maintain LSECs fenestrae via activating the PI3K-AKT-MTOR pathway. Additionally, inhibiting autophagy, such as 3MA, bafilomycin, or ATG5-siRNA, could attenuate the depletion of Cav-1 and F-actin remodeling to maintain LSECs fenestrae and improve the NO-dependent pathway; in turn, eNOS-siRNA and L-NAME, for blocking the NO-dependent pathway, could elevate autophagic degradation of Cav-1 to aggravate defenestration. Finally, overexpressed Cav-1 rescued rapamycin-induced autophagic degradation of Cav-1 to maintain LSECs fenestrae; whereas knockdown of Cav-1 facilitated defenestration due to the activation of the AMPK-dependent autophagy. Consequently, autophagic degradation of Cav-1 promotes LSECs defenestration via inhibiting the NO-dependent pathway and F-actin remodeling.
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