Fig. 2: Effect of growth factors on AKI and AKI-CKD progression. | Signal Transduction and Targeted Therapy

Fig. 2: Effect of growth factors on AKI and AKI-CKD progression.

From: Potential targeted therapy and diagnosis based on novel insight into growth factors, receptors, and downstream effectors in acute kidney injury and acute kidney injury-chronic kidney disease progression

Fig. 2

Many growth factors, such as BMP-7, EGF, FGF-2, HGF, IGF-1, VEGF, and TGF-β1, are involved in the programmed cell death of endothelial or epithelial cells in the acute injury phase. BMP-7, FGF-2, HGF, TGF-β1, and IGF-1 participate in the regulation of the inflammatory microenvironment that is responsible for cytokine production and immune cell recruitment. TGF-β1 is a double-edged growth factor. In addition, TGF-β1 exerts anti-inflammatory effects, and TGF-β1 overproduction leads to acute tubular injury. After injured epithelial cells fail to regenerate through differentiation, fibrosis is induced as a self-limiting repair process to limit damage. In this stage, overproduction of growth factors such as TGF-β1, PDGF, and FGF induces fibroblast/pericyte proliferation, transdifferentiation of tubular epithelial cells, endothelial cells, and macrophages, and extracellular matrix production, leading to CKD. Concurrently, abnormal synthesis of PDGF-B, VEGF, EGF, and TGF-β1 has a negative impact on endothelial integrity and causes capillary rarefaction, accelerating renal fibrosis.

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