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However, evidence suggests that this process may be reversible, making it a potential therapeutic target for mitigating renal injury ( Further studies on chronic kidney damage models, such as diabetic kidney disease, reveal that podocyte depletion occurs due to the exposure of glomeruli to harmful stimuli, OS inducers such as hyperglycemia, hyperuremia, increased levels of fatty acids, growth factors, cytokines, and hormones ( In this sense, it is noted that targeting cellular pathways involved in OS dynamics (e.g., modulation of the TSP-1/TGF-1/Smad pathway by overexpression of Sestrin2) protects podocytes from apoptosis

doi: 10.3389/fendo.2021.721135 10

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