Oncotarget

Reviews:

Cellular senescence, senescence-associated secretory phenotype, and chronic kidney disease

Wen-Juan Wang _, Guang-Yan Cai and Xiang-Mei Chen

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Oncotarget. 2017; 8:64520-64533. https://doi.org/10.18632/oncotarget.17327

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Abstract

Wen-Juan Wang1,2, Guang-Yan Cai1 and Xiang-Mei Chen1

1Department of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing 100853, China

2Department of Nephrology, Beijing Changping Hospital, Beijing 102200, China

Correspondence to:

Guang-Yan Cai, email: [email protected]

Keywords: chronic kidney disease, cellular senescence, senescence-associated secretory phenotype, CKD-associated secretory phenotype

Received: February 08, 2017     Accepted: March 24, 2017     Published: April 21, 2017

ABSTRACT

Chronic kidney disease (CKD) is increasingly being accepted as a type of renal ageing. The kidney undergoes age-related alterations in both structure and function. To date, a comprehensive analysis of cellular senescence and senescence-associated secretory phenotype (SASP) in CKD is lacking. Hence, this review mainly discusses the relationship between the two phenomena to show the striking similarities between SASP and CKD-associated secretory phenotype (CASP). It has been reported that replicative senescence, stress-induced premature ageing, and epigenetic abnormalities participate in the occurrence and development of CKD. Genomic damage and external environmental stimuli cause increased levels of oxidative stress and a chronic inflammatory state as a result of irreversible cell cycle arrest and low doses of SASP. Similar to SASP, CASP factors activate tissue repair by multiple mechanisms. Once tissue repair fails, the accumulated SASP or CASP species aggravate DNA damage response (DDR) and cause the senescent cells to secrete more SASP factors, accelerating the process of cellular ageing and eventually leading to various ageing-related changes. It is concluded that cellular senescence and SASP participate in the pathological process of CKD, and correspondingly CKD accelerated the progression of cell senescence and the secretion of SASP. These results will facilitate the integration of these mechanisms into the care and management of CKD and other age-related diseases.


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