Youming Peng

TL;DR: CKD is associated with significant changes in cell signaling in kidney tissues, including the activation of transforming growth factor-β, p53, hypoxia-inducible factor, and major developmental pathways, which may contribute to the heightened sensitivity of, and nonrecovery from, AKI.

TL;DR: It is shown thatmitophagy is induced in renal proximal tubular cells in both in vitro and in vivo models of ischemic AKI, indicating that PINK1-PARK2-mediated mitophagy plays an important role in mitochondrial quality control, tubular cell survival, and renal function during AKI.

TL;DR: This study revealed the persistent activation of mammalian target of rapamycin (mTOR) signaling in the interstitial macrophages and myofibroblasts, but rarely in injured proximal epithelial cells, CD4+ T cells, neutrophils, or endothelial cells during the development of kidney fibrosis.

TL;DR: Mechanisms by which p66Shc mediates HG- and ANG II-induced mitochondrial dysfunctions via PKC-β and Pin1-dependent pathways in renal tubular cells are investigated.

TL;DR: This review proposes experimental strategies for the identification of renoprotective agents or methods with clinical potential in acute kidney injury and proposes the consideration of combination therapy by targeting multiple targets in AKI.