Year: 2025
Type: article
Abstract: Podocytes are highly specialized, terminally differentiated epithelial cells essential for maintaining the glomerular filtration barrier. Their limited regenerative capacity and high metabolic demands render them particularly susceptible to aging-related stress. Accumulating evidence indicates that podocyte aging, characterized by cellular senescence, mitochondrial dysfunction, autophagy impairment, and epigenetic alterations, significantly contributes to the pathogenesis of diverse glomerular diseases collectively termed podocytopathies. These include focal segmental glomerulosclerosis, membranous nephropathy, minimal change disease, diabetic kidney disease, and lupus nephritis. This review discusses the cellular and molecular mechanisms driving podocyte aging and explores how these alterations predispose to podocyte injury, loss, and dysfunction, ultimately culminating in podocytopathies. Furthermore, we highlight current and emerging therapeutic strategies that aim to preserve podocyte health by targeting aging-associated pathways. Understanding podocyte aging elucidates mechanisms of chronic kidney disease progression and identifies novel therapeutic strategies for age-specific interventions in podocytopathies.
DOI: 10.3390/ijms26189159
Authors: Si-Jia Ma, Yu-Ting Zhu, Fang-Fang He, Chun Zhang
Institution: Huazhong University of Science and Technology
Language: English
Subfield: Nephrology
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,499
OpenAlex ID: W4414579102