Figure 1.

Phenotypic changes described in TECs following IRI associated with maladaptive tubular repair and progressive renal interstitial fibrosis. These changes include but are not limited to: cell damage (chronic inflammation with persistent cytokine production and immune cell infiltrate), mitochondrial dysfunction and cell death (enhanced ROS signaling, metabolic reprogramming, and release of mitochondrial DNA/ROS acting as danger molecules, ultimately leading to cell death). Lastly, as a result of incomplete repair or severe damage, TECs can undergo transient cell cycle arrest, as a protective mechanism to ensure genome stability. However, if persistent, this leads to a pro-inflammatory and profibrotic secretome, ultimately leading to fibrosis.