ArticleRedox biology2017
Caveolin 1-related autophagy initiated by aldosterone-induced oxidation promotes liver sinusoidal endothelial cells defenestration.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Dietary, Nutrient, and Supramolecular Nanofiber Modulation of the Liver Sinusoidal Clearance System in Metabolic Diseases and Aging.Biomedicines · 2026Review
- Mineralocorticoid Receptor Antagonists for Liver Fibrosis: Potential Mechanisms and Research Progress.Journal of clinical and translational hepatology · 2026Review
- Mechanical mechanics-reclaiming a new battlefield for chronic liver disease.Journal of advanced research · 2026Review
- Cell-specific roles of autophagy in liver fibrosis: implications for targeted pharmacotherapy.Annals of medicine · 2025Review
- Defenestration of Liver Sinusoidal Endothelial Cells: The Trigger of Liver Fibrosis.Pharmaceuticals (Basel, Switzerland) · 2025Review
- EGCG suppressed activation of hepatic stellate cells by regulating the PLCE1/IPEuropean journal of nutrition · 2024Article
- Interplay between caveolin-1 and mineralocorticoid receptor in cardiometabolic disease.The Journal of endocrinology · 2024Review
- Endothelial cell serum and glucocorticoid regulated kinase 1 (SGK1) mediates vascular stiffening.Metabolism: clinical and experimental · 2024Article
- Autophagic degradation of MVBs in LSECs promotes Aldosterone induced-HSCs activation.Hepatology international · 2024Article
- 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
- Protein components of maple syrup as a potential resource for the development of novel anti‑colorectal cancer drugs.Oncology reports · 2023Article
- Maternal hepatic immunology during pregnancy.Frontiers in immunology · 2023Review
- Article
- Caveolin-1 scaffolding domain peptide abrogates autophagy dysregulation in pulmonary fibrosis.Scientific reports · 2022Article
- Icariside Ⅱ Attenuates Palmitic Acid-Induced Endothelial Dysfunction Through SRPK1-Akt-eNOS Signaling Pathway.Frontiers in pharmacology · 2022Article
- Review
- Sirtuin 1 ameliorates defenestration in hepatic sinusoidal endothelial cells during liver fibrosis via inhibiting stress-induced premature senescence.Cell proliferation · 2021Article
- Klotho as Potential Autophagy Regulator and Therapeutic Target.Frontiers in pharmacology · 2021Review
- Aldosterone enhances high phosphate-induced vascular calcification through inhibition of AMPK-mediated autophagy.Journal of cellular and molecular medicine · 2020Article
- Twist1-induced miR-199a-3p promotes liver fibrosis by suppressing caveolin-2 and activating TGF-β pathway.Signal transduction and targeted therapy · 2020Article
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aldosterone, with pro-oxidation and pro-autophagy capabilities, plays a key role in liver fibrosis. However, the mechanisms underlying aldosterone-promoted liver sinusoidal endothelial cells (LSECs) defenestration remain unknown. Caveolin 1 (Cav1) displays close links with autophagy and fenestration. Hence, we aim to investigate the role of Cav1-related autophagy in LSECs defenestration. We found the increase of aldosterone/MR (mineralocorticoid receptor) level, oxidation, autophagy, and defenestration in LSECs in the human fibrotic liver, BDL or hyperaldosteronism models; while antagonizing aldosterone or inhibiting autophagy relieved LSECs defenestration in BDL-induced fibrosis or hyperaldosteronism models. In vitro, fenestrae of primary LSECs gradually shrank, along with the down-regulation of the NO-dependent pathway and the augment of the AMPK-dependent autophagy; these effects were aggravated by rapamycin (an autophagy activator) or aldosterone treatment. Additionally, aldosterone increased oxidation mediated by Cav1, reduced ATP generation, and subsequently induced the AMPK-dependent autophagy, leading to the down-regulation of the NO-dependent pathway and LSECs defenestration. These effects were reversed by MR antagonist spironolactone, antioxidants or autophagy inhibitors. Besides, aldosterone enhanced the co-immunoprecipitation of Cav1 with p62 and ubiquitin, and induced Cav1 co-immunofluorescence staining with LC3, ubiquitin, and F-actin in the perinuclear area of LSECs. Furthermore, aldosterone treatment increased the membrane protein level of Cav1, whereas decrease the cytoplasmic protein level of Cav1, indicating that aldosterone induced Cav1-related selective autophagy and F-actin remodeling to promote defenestration. Consequently, Cav1-related selective autophagy initiated by aldosterone-induced oxidation promotes LSECs defenestration via activating the AMPK-ULK1 pathway and inhibiting the NO-dependent pathway.
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