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.
Highlights
The continuous accumulation of senescent cells leads to the age-related deterioration of vital organs and constitutes an organism's ageing process
It is concluded that cellular senescence and senescence-associated secretory phenotype (SASP) participate in the pathological process of Chronic kidney disease (CKD), and correspondingly CKD accelerated the progression of cell senescence and the secretion of SASP
Consistent with angiotensin receptor blockers, growth factors such as FGF23 can significantly reduce the levels of inflammation and oxidative stress and further decrease renal fibrosis and lipid metabolic disorders during the progress of diabetic nephropathy, mainly by blocking the renin-angiotensin-aldosterone system (RAAS), enhancing the expression of Klotho, and inhibiting the expression of monocyte chemotactic protein-1 (MCP-1)/Tumor necrosis factor-α (TNF-α) and transforming growth factor-β (TGF-β) [81, 82]
Summary
The continuous accumulation of senescent cells leads to the age-related deterioration of vital organs and constitutes an organism's ageing process. 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.
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