Cellular senescence promotes macrophage-to-myofibroblast transition in chronic ischemic renal disease.

Yu Zhao, Xiang-Yang Zhu, Wenqi Ma, Ying Zhang, Fei Yuan, Seo Rin Kim, Hui Tang, Kyra Jordan, Amir Lerman, Tamara Tchkonia, James L Kirkland, Lilach O Lerman

Institute of Nephrology, Zhong Da Hospital, Southeast University, School of Medicine, Nanjing, Jiangsu, PR China.Institute of Nephrology, Zhong Da Hospital, Southeast University, School of Medicine, Nanjing, Jiangsu, PR China. · pubmed

Paper

Abstract

Cellular senescence participates in the pathophysiology of post-stenotic kidney damage, but how it regulates tissue remodeling is incompletely understood. Macrophage-myofibroblast transition (MMT) contributes to the development of tissue fibrosis. We hypothesized that cellular senescence contributes to MMT and renal fibrosis in mice with renal artery stenosis (RAS). INK-ATTAC mice expressing p16

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Research summary

Cellular senescence contributes to macrophage-to-myofibroblast transition and renal fibrosis in chronic ischemic renal disease. This research addresses the role of cellular senescence in tissue remodeling, which is a key aspect of aging and age-related diseases, thus linking it to the broader context of longevity.

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