Renal inflammaging: Mechanisms, pathophysiology and therapeutic prospects.
Abstract
The ageing global population faces a rising prevalence of chronic kidney disease (CKD), now recognized as a state of accelerated ageing driven by chronic low-grade inflammation-inflammaging. This review synthesizes current evidence positioning the kidney not merely as a passive target but as an active participant in systemic inflammaging, a process fueled by immunosenescence, metabolic reprogramming, and cellular senescence. We explore how resident renal cells, including tubular epithelial cells, podocytes, and mesangial cells, adopt a senescence-associated secretory phenotype (SASP) that perpetuates inflammation, fibrosis, and functional decline. Key mechanisms (NLRP
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Research summary
The paper claims that renal cells contribute to systemic inflammaging through mechanisms like SASP, which perpetuates inflammation and functional decline. This research is relevant as it addresses the underlying mechanisms of aging and chronic kidney disease, focusing on the role of inflammation in the aging process.
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