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Updated: May 25, 2025
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Published on: April 25, 2025
Update of cellular senescence in kidney fibrosis: from mechanism to potential interventions
Lina Yang1, Liang Ma1, Ping Fu1
1Department of Nephrology, Institute of Kidney Diseases, West China Hospital of Sichuan University, Chengdu, 610041, China.
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.
Insights
Aging accelerates kidney fibrosis, a hallmark of chronic kidney disease (CKD). This review explores how cellular senescence contributes to kidney fibrosis and discusses senolytic therapies to slow CKD progression.
Area of Science:
- Nephrology
- Gerontology
- Cellular Biology
Background:
- Kidney fibrosis is the common endpoint for chronic kidney disease (CKD).
- Aging is a significant risk factor for CKD.
- Senescent cells are present in aging kidneys and contribute to CKD.
Purpose of the Study:
- To review the role of cellular senescence in kidney fibrosis.
- To discuss the mechanisms by which senescent cells promote kidney fibrosis.
- To evaluate senolytic therapies for mitigating kidney fibrosis.
Main Methods:
- Literature review of studies on kidney fibrosis and cellular senescence.
- Analysis of epidemiological, clinical, and molecular evidence.
- Discussion of potential therapeutic strategies targeting senescent cells.
Main Results:
- Accumulating evidence implicates cellular senescence in the pathogenesis of kidney fibrosis.
- Senescent cells in the kidney contribute to fibrosis through various mechanisms.
- Targeting senescent cells may offer a novel therapeutic approach for CKD.
Conclusions:
- Cellular senescence is a key driver of kidney fibrosis in CKD.
- Further research is needed to elucidate the precise mechanisms.
- Senolytic therapies hold promise for treating kidney fibrosis and slowing CKD progression.
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