Targeting tumor suppressor p53 for organ fibrosis therapy

被引：0

作者：

Bao, Yi-Ni ^{[1
]}

Yang, Qiao ^{[1
]}

Shen, Xin-Lei ^{[1
]}

Yu, Wen-Kai ^{[1
]}

Zhou, Li ^{[1
]}

Zhu, Qing-Ru ^{[1
]}

Shan, Qi-Yuan ^{[1
]}

Wang, Zhi-Chao ^{[1
]}

Cao, Gang ^{[1
]}

机构：

[1] Zhejiang Chinese Med Univ, Sch Pharm, 548 Binwen Rd, Hangzhou 310053, Zhejiang, Peoples R China

来源：

CELL DEATH & DISEASE | 2024年 / 15卷 / 05期

基金：

中国国家自然科学基金;

关键词：

HEPATIC STELLATE CELLS; DNA-DAMAGE RESPONSES; MESENCHYMAL TRANSITION; CELLULAR SENESCENCE; APOPTOSIS; PROMOTES; CYCLE; NANOPARTICLE; PATHOGENESIS; ACETYLATION;

D O I：

10.1038/s41419-024-06702-w

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Fibrosis is a reparative and progressive process characterized by abnormal extracellular matrix deposition, contributing to organ dysfunction in chronic diseases. The tumor suppressor p53 (p53), known for its regulatory roles in cell proliferation, apoptosis, aging, and metabolism across diverse tissues, appears to play a pivotal role in aggravating biological processes such as epithelial-mesenchymal transition (EMT), cell apoptosis, and cell senescence. These processes are closely intertwined with the pathogenesis of fibrotic disease. In this review, we briefly introduce the background and specific mechanism of p53, investigate the pathogenesis of fibrosis, and further discuss p53's relationship and role in fibrosis affecting the kidney, liver, lung, and heart. In summary, targeting p53 represents a promising and innovative therapeutic approach for the prevention and treatment of organ fibrosis.

引用

页数：11

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