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. 2023 May 11;42(6):686–699. doi: 10.23876/j.krcp.23.001

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Copyright © 2023 The Korean Society of Nephrology

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial and No Derivatives License (http://creativecommons.org/licenses/by-nc-nd/4.0/) which permits unrestricted non-commercial use, distribution of the material without any modifications, and reproduction in any medium, provided the original works properly cited.

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Figure 2. — (1) Renal tubular epithelium cell-cycle arrest, (2) epigenetic change, (3) chronic inflammation, (4) dysfunction of mitochondria, (5) failed regeneration of tubular cells, (6) endothelial dysfunction, (7) metabolic reprogramming, and (8) RAS activation.

AGT, angiotensinogen; AKI, acute kidney disease; ANG I, angiotensin I; ANG II, angiotensin II; AT1R, angiotensin type-1 receptor; FAO, fatty acid β-oxidation; IL, interleukin; RAS, renin-angiotensin system; ROS, reactive oxygen species; TNF-α, tumor necrosis factor α.