ArticleMolecular and cellular biochemistry2020
Trehalose attenuates TGF-β1-induced fibrosis of hSCFs by activating autophagy.
Article in Molecular and cellular biochemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- [Silybin inhibits fibrosis after glaucoma filtration surgery in rabbits by promoting fibroblast autophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- The role of myocardial fibrosis in the diabetic cardiomyopathy.Diabetology & metabolic syndrome · 2025Review
- Tibetan medicine Pa Zhu Wan ameliorates carbon tetrachloride-induced liver fibrosis in rats by regulating the TGF-β-Smad2/3 and IL-6/JAK2/STAT3 signaling pathways.Frontiers in pharmacology · 2025Article
- Autophagy activation ameliorates the fibrosis of trabecular meshwork cells induced by TGFβ2 through the promotion of fibrotic proteins degradation.Human cell · 2024Article
- Trehalose Rescues Postmenopausal Osteoporosis Induced by Ovariectomy through Alleviating Osteoblast Pyroptosis via Promoting Autophagy.Biomedicines · 2024Article
- Article
- Epigallocatechin-3-gallate attenuates myocardial fibrosis in diabetic rats by activating autophagy.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Nampt promotes fibroblast extracellular matrix degradation in stress urinary incontinence by inhibiting autophagy.Bioengineered · 2022Article
- miR221 regulates TGF-β1-induced HSC activation through inhibiting autophagy by directly targeting LAMP2.Molecular medicine reports · 2021Article
- Review
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Conjunctival fibrosis is a process of extracellular matrix accumulation and the appearance of myofibroblasts in subconjunctival fibroblasts induced by injury or inflammation, which can significantly reduce the filtration efficiency of glaucoma filtration surgery. In this study, autophagy was confirmed to be involved in regulating the fibrosis of human subconjunctival fibroblasts (hSCFs) induced by TGF-β1. Following the addition of rapamycin, we detected that autophagy activation could reduce the increased expression level of αSMA and the accumulation of extracellular matrix component proteins namely fibronectin and type I collagen induced by TGF-β1 via the inhibition of SMAD2 phosphorylation. Following the addition of HCQ, the inhibition of autophagy aggravated TGF-β1-induced fibrosis of hSCFs. We further verified that trehalose, a safe clinical drug, could alleviate TGF-β1-induced fibrosis of hSCFs by activating autophagy and that these effects could be blocked by autophagy inhibition. In summary, autophagy was shown to be involved in the regulation of TGF-β1-induced fibrosis of hSCFs, which provided a novel perspective for exploring the progression of this lesion. More importantly, the protective effects of trehalose on TGF-β1-induced fibrosis of hSCFs were mediated by the activation of autophagy and could provide possible new approaches for the clinical treatment of conjunctival fibrosis.
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