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. 2023 Sep 13;24(18):14019. doi: 10.3390/ijms241814019

Figure 1.

Figure 1

Pathogenic mechanisms involved in AKI transition to CKD. The mentioned risk factors prone AKI subjects to higher glomerular and/or tubule-interstitial system cellular damage. Furthermore, apoptotic, necrotic and senescent cells (cells blocked in the G2/M cell cycle) release and stimulate pro-fibrotic factors, which, via FMT, PMT, EMT, EndMT and MMT, will generate myofibroblasts. Myofibroblasts secrete ECM that will generate glomerulosclerosis, tubulointerstitial fibrosis and arteriosclerosis, defined as CKD. Acronyms: AKI—acute kidney injury; CKD—chronic kidney disease; CTGF—connective tissue growth factor; ECM—extracellular matrix; EGF—epidermal growth factor; EMT—epithelial to mesenchymal transition; EndMT—endothelial to mesenchymal transition; FMT—fibroblast to myofibroblast transition; HIF—hypoxia-inducible factor; KDIGO—Kidney Disease Improving Global Outcomes; IL—interleukin; MMP-7—matrix metalloproteinase-7; MMT—macrophage myofibroblast transition; mTOR—mammalian target of rapamycin; Notch—neurogenic locus notch homolog protein; PDGF—platelet-derived growth factor; PGF—placental growth factor; PMT—pericyte to myofibroblast-transition; RAS—renin-angiotensin system; RNAs—ribonucleic acids; TGF-β1—transforming growth factor; TIMP—tissue inhibitor of metalloproteinase; TNF-α—tumor necrosis factor alpha; TWEAK—TNF-like weak inducer of apoptosis; VEGF—vascular endothelial growth factor; Wnt/β-catenin—wingless/beta-catenin.