Update of cellular senescence in kidney fibrosis: from mechanism to potential interventions.
10.1007/s11684-024-1117-z
- Author:
Lina YANG
1
;
Liang MA
1
;
Ping FU
1
;
Jing NIE
2
Author Information
1. Department of Nephrology, Institute of Kidney Diseases, West China Hospital of Sichuan University, Chengdu, 610041, China.
2. Biobank of Peking University First Hospital, Peking University First Hospital, State Key Laboratory of Vascular Homeostasis and Remodeling, Health Science Center, Peking University, Beijing, 100034, China. niejing@pkufh.com.
- Publication Type:Review
- Keywords:
SASP;
cell cycle arrest;
cellular senescence;
kidney fibrosis;
senolytics;
senomorphics
- MeSH:
Humans;
Cellular Senescence/physiology*;
Fibrosis;
Renal Insufficiency, Chronic/pathology*;
Kidney/pathology*;
Animals
- From:
Frontiers of Medicine
2025;19(2):250-264
- CountryChina
- Language:English
-
Abstract:
Kidney fibrosis is the final common pathway of virtually all chronic kidney disease (CKD). However, despite great progress in recent years, no targeted antifibrotic therapies have been approved. Epidemiologic, clinical, and molecular evidence suggest that aging is a major contributor to the increasing incidence of CKD. Senescent renal tubular cells, fibroblasts, endothelial cells, and podocytes have been detected in the kidneys of patients with CKD and animal models. Nonetheless, although accumulated evidence supports the essential role of cellular senescence in CKD, the mechanisms that promote cell senescence and how senescent cells contribute to CKD remain largely unknown. In this review, we summarize the features of the cellular senescence of the kidney and discuss the possible functions of senescent cells in the pathogenesis of kidney fibrosis. We also address whether pharmacological approaches targeting senescent cells can be used to retard the the progression of kidney fibrosis.
