During recovery by regeneration after AKI, proximal tubule cells can fail to redifferentiate,
undergo premature growth arrest, and become atrophic. The atrophic tubules display
pathologically persistent signaling increases that trigger production of profibrotic peptides,
proliferation of interstitial fibroblasts, and fibrosis. We studied proximal tubules after ischemia-
reperfusion injury (IRI) to characterize possible mitochondrial pathologies and alterations of
critical enzymes that govern energy metabolism. In rat kidneys, tubules undergoing atrophy …