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Targeting SIRT2 in Aging-Associated Fibrosis Pathophysiology
Yongjiao Huang1,2,3, Wei He1,3,4, Yingting Zhang1
1Department of Pathophysiology, Key Laboratory of Cell Differentiation and Apoptosis of Ministry of Education, Shanghai Frontiers Science Center of Cellular Homeostasis and Human Diseases, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Aging accelerates fibrosis by accumulating senescent cells. Sirtuin 2 (SIRT2), a key enzyme, plays a vital role in liver, kidney, and heart fibrosis during aging, offering a potential therapeutic target.
Area of Science:
- Biogerontology
- Cellular Biology
- Pathology
Background:
- Aging is a complex process linked to chronic diseases and tissue fibrosis.
- Senescent cell accumulation disrupts tissue microenvironments, promoting fibrosis.
- Fibrosis arises from abnormal tissue repair in chronic inflammatory conditions.
Purpose of the Study:
- To summarize the role of Sirtuin 2 (SIRT2) in aging-related fibrosis.
- To explore SIRT2 as a potential therapeutic target for anti-fibrotic drugs.
Main Methods:
- Literature review focusing on aging, fibrosis, and SIRT2.
- Analysis of SIRT2's involvement in liver, kidney, and cardiac fibrosis.
Main Results:
- SIRT2, a NAD+-dependent histone deacetylase, is highly expressed in aging tissues.
- SIRT2 activity is implicated in the progression of liver, kidney, and cardiac fibrosis.
- Modulating SIRT2 may offer a strategy to combat age-related fibrosis.
Conclusions:
- SIRT2 is a critical regulator in the development of fibrosis during aging.
- Targeting SIRT2 presents a promising avenue for developing novel anti-fibrotic therapies.
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