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ORIGINAL RESEARCH article

Front. Med.
Sec. Ophthalmology
Volume 11 - 2024 | doi: 10.3389/fmed.2024.1534120
This article is part of the Research Topic New Concepts, Advances, and Future Trends in Clinical Research on Eye Diseases View all 14 articles

Aging-enhanced autophagy activity promotes fibrotic progression via the TGF-β2/Smad signaling pathway in trabecular meshwork cells-a new insight from POAG

Provisionally accepted
Jin Han Jin Han 1*Jun Wang Jun Wang 1Ling Shen Ling Shen 2*Yiting Cai Yiting Cai 1*Eric Wang Eric Wang 1Ailixiati Wumaier Ailixiati Wumaier 1*Wei Han Wei Han 1*Wei Chen Wei Chen 3*
  • 1 Eye Center, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
  • 2 Stomatology Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China
  • 3 Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, China

The final, formatted version of the article will be published soon.

    Glaucoma, a leading cause of irreversible blindness, is characterized by optic neuropathy and retinopathy, with primary open-angle glaucoma (POAG) being the most prevalent form. The primary pathogenic mechanism of POAG is the elevation of intraocular pressure due to the chronic fibrosis of the trabecular meshwork (TM). Autophagy plays a key role in maintaining cellular homeostasis and is involved in the progression of fibrosis in various organs. However, the exact contribution of autophagy to fibrosis related to POAG pathogenesis remains unknown. This study reveals increased autophagic activity in tissues from POAG patients and an age-related upregulation of autophagy in healthy human TM tissues. Using chronic H2O2 treatment as an aging model, we observed autophagy induction and fibrosis in TM cells. We further examined the role of autophagy in fibrosis and found that enhanced autophagy activity promoted fibrotic progression via the TGF-β2/Smad signaling pathway.Dexamethasone-treated TM cells served as a POAG model, highlighting the enhancing role of autophagy in fibrosis. Our work casts light on the mechanism of POAG fibrogenesis and may aid in developing potential targets for clinical therapy.

    Keywords: POAG, Autophagy, Aging, Trabecular Meshwork, Fibrosis

    Received: 25 Nov 2024; Accepted: 30 Dec 2024.

    Copyright: © 2024 Han, Wang, Shen, Cai, Wang, Wumaier, Han and Chen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Jin Han, Eye Center, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
    Ling Shen, Stomatology Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, Zhejiang Province, China
    Yiting Cai, Eye Center, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
    Ailixiati Wumaier, Eye Center, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
    Wei Han, Eye Center, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
    Wei Chen, Institute of Immunology, Zhejiang University School of Medicine, Hangzhou, 310058, Zhejiang Province, China

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