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. 2022 Oct 21;13:991059. doi: 10.3389/fphar.2022.991059

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Copyright © 2022 Sharma and Patial.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Role of PPAR-γ in the pathophysiology of kidney diseases. The suppression of PPAR-γ in disease conditions further activates the inflammatory and fibrogenic factors leading to kidney damage. AGE, Advanced glycation end products; BAX, BCL2-associated X protein; BCL-2, B-cell leukemia/lymphoma 2; CAT, Catalase; GPx, Glutathione peroxidase; GFR, Glomerular filtration rate; IL-6, Interleukin-6; IL-1β, Interleukin-1 β, IgA1, Immunoglobulins A1; MCP1, Monocyte chemoattractant protein-1; NFκB, Nuclear factor-kappa B light-chain-enhancer of activated B cells; NO, Nitric oxide; NrF2, Nuclear factor-erythroid factor 2-related factor 2; ROS, Reactive oxygen species; RAAS, Renin-Angiotensin-Aldosterone System; SOD, Superoxide dismutase; STAT, Signal transducer and activator of transcription; TGFβ, Transforming growth factor-beta; TNFα, Tumor necrosis factor-alpha.