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<p>Age-related glomerulosclerosis is a notably characterized by a significant decrease in both the quantity and density of podocytes. Aging podocytes undergo cytoskeletal remodeling, lose their foot processes, and their adherence to the glomerular basement membrane (GBM). Consequently, they fail to form a complete membrane structure with adjacent podocytes, triggering proteinuria and diverse kidney diseases. This is particularly prominent during unhealthy aging, further intensified by comorbid conditions like obesity or diabetes. Aging and related diseases result in a reduction in podocyte number, cytoskeleton rearrangement, and the disappearance and shedding of the foot processes. These processes share numerous common factors and are controlled by multiple mechanisms, which exhibit both overlap and complementarity. Due to the high costs and time-consuming nature of healthy aging research, most current studies focusing on podocyte senescence have utilized stimulatory techniques such as high sugar, oxidative stress, inflammation, and among others, to optimize a more efficient model that demonstrates accelerated podocyte aging. This review primarily summarizes the mechanisms underlying podocyte injury in pathologic aging induced by metabolic/environmental factors and the consequences of the kidney (Fig.&#xa0;1). It also extracts potential research targets from these mechanisms, aiming to provide therapeutic strategies that can alleviate podocyte injury, delay kidney aging, and sustain normal kidney function.</p>

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Potential targets of protecting podocyte in glomerular aging and injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年6月17日

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  • Ziying Zhong

摘要

Age-related glomerulosclerosis is a notably characterized by a significant decrease in both the quantity and density of podocytes. Aging podocytes undergo cytoskeletal remodeling, lose their foot processes, and their adherence to the glomerular basement membrane (GBM). Consequently, they fail to form a complete membrane structure with adjacent podocytes, triggering proteinuria and diverse kidney diseases. This is particularly prominent during unhealthy aging, further intensified by comorbid conditions like obesity or diabetes. Aging and related diseases result in a reduction in podocyte number, cytoskeleton rearrangement, and the disappearance and shedding of the foot processes. These processes share numerous common factors and are controlled by multiple mechanisms, which exhibit both overlap and complementarity. Due to the high costs and time-consuming nature of healthy aging research, most current studies focusing on podocyte senescence have utilized stimulatory techniques such as high sugar, oxidative stress, inflammation, and among others, to optimize a more efficient model that demonstrates accelerated podocyte aging. This review primarily summarizes the mechanisms underlying podocyte injury in pathologic aging induced by metabolic/environmental factors and the consequences of the kidney (Fig. 1). It also extracts potential research targets from these mechanisms, aiming to provide therapeutic strategies that can alleviate podocyte injury, delay kidney aging, and sustain normal kidney function.