The emerging role of cellular senescence in renal diseases.

Rong Chen,Ying Wan,Bingru Zhou,Nan Wu,Heather Francis,Ping Zou,Shannon Glaser,Chunmei Zhang,Gianfranco Alpini,Siwen Li,Xuesen Li,Fanyin Meng,Tianhao Zhou

doi:10.1111/jcmm.14952

Abstract

Cellular senescence represents the state of irreversible cell cycle arrest during cell division. Cellular senescence not only plays a role in diverse biological events such as embryogenesis, tissue regeneration and repair, ageing and tumour occurrence prevention, but it is also involved in many cardiovascular, renal and liver diseases through the senescence‐associated secretory phenotype (SASP). This review summarizes the molecular mechanisms underlying cellular senescence and its possible effects on a variety of renal diseases. We will also discuss the therapeutic approaches based on the regulation of senescent and SASP blockade, which is considered as a promising strategy for the management of renal diseases.

Highlights

Cellular senescence refers to an irreversible cell cycle arrest
Enhanced cellular senescence is found in multiple organs in the process of ageing or after injury, suggesting that there should be different effects of cellular senescence depending on the pathophysiological context.[5]
It has been shown that mitotic arrest at the G2/M phase plays a crucial role in response to AKI, where it drives maladaptive repair and progressive fibrosis; this suggests that renal recovery after injury would be hampered due to increased numbers of senescent cells and reduced regenerative capacity of aged kidneys

Summary

Introduction

Cellular senescence refers to an irreversible cell cycle arrest. Senescent cells exhibit a series of changes in cell morphology and epigenetics, including the changes in cell cyclins and increased expression of β-galactosidase[1]; there is replicative exhaustion in senescent cells, these cells still have metabolic activity.[1].

Results

Conclusion