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Chaperone-mediated autophagy supports organ regeneration and fibroblast quiescence in mouse models of fibrosis

ABSTRACT: Chaperone-mediated autophagy (CMA) acting as a crucial, selective protein degradation pathway is a key topic in understanding tissue remodeling and disease, with recent research showing its pivotal role in maintaining organ health, particularly through the maintenance of fibroblast quiescence and supporting regeneration in fibrosis models.

ORGANISM(S): Mus Musculus

SUBMITTER: Jiazhen Wang

PROVIDER: PXD073386 | iProX | Thu Jan 22 00:00:00 GMT 2026

REPOSITORIES: iProX

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Chaperone-mediated autophagy supports organ regeneration and fibroblast quiescence in mouse models of fibrosis.

Wang Jiazhen J Wang Ru R Liu Yang Y Li Yicun Y Xian Peng P Zhang Yuanhang Y Zhang Xinning X Wang Jiayi J Tu Chuangeng C Zhang Haojian H Li Jiansheng J

Science translational medicine 20260218 837

The core of organ fibrosis formation lies in the regenerative defects of parenchymal cells and in the excessive activation of fibroblasts, yet methods to simultaneously address these pathological cell types remain lacking. Here, we found that the expression of the chaperone-mediated autophagy (CMA) limiting factor lysosome-associated membrane protein type 2A (LAMP2A) was consistently down-regulated in mouse models of bleomycin-induced pulmonary fibrosis, carbon tetrachloride (CCl<sub>4</sub>)-in ...[more]

PMID: 41706873

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