Cellular Senescence in Metabolic-Associated Kidney Disease: An Update

Abstract

Cellular senescence is described as the state where the cell cycle is arrested irreversibly, which occurs in response to various forms of stress factors in cells, leading to the senescence-associated secretory phenotype (SASP). We can assess the accumulation of senescent cells in tissues or organs through biomarkers of cellular senescence such as p16INK4a, p53, p21, and SA-β-GAL. In recent decades, a large number of studies have reported the biomarkers of increased cell senescence in pathogenic tissues, demonstrating the possible connection between cell senescence and various diseases. Kidney damage often occurs in the pathophysiological process of certain metabolic diseases, resulting in metabolic-associated kidney diseases. For example, hypertension causes systemic arteriosclerosis, and the kidney can be seriously affected by abundant blood vessels, which may lead to a decreased glomerular filtration rate (GFR) and proteinuria, resulting in hypertension-related kidney diseases. The accumulation of senescent cells may also be observed in some metabolic-associated kidney diseases (such as obesity-related nephropathy, hypertension-related nephropathy, and diabetic nephropathy). In this paper, we review existing knowledge regarding the influence of cellular senescence on metabolic-associated kidney diseases, providing new ideas for future treatment.