Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD

By D. Ferenbach, Joseph V. Bonventre. Nature Reviews Nephrology, 2015

824 citations recorded by the source corpus.

Acute kidney injury is an increasingly common complication of hospital admission and is associated with high levels of morbidity and mortality. A hypotensive, septic, or toxic insult can initiate a cascade of events, resulting in impaired microcirculation, activation of inflammatory pathways and tubular cell injury or death. These processes ultimately result in acutely impaired kidney function and initiation of a repair response. This Review explores the various mechanisms responsible for the initiation and propagation of acute kidney injury, the prototypic mechanisms by which a substantially damaged kidney can regenerate its normal architecture, and how the adaptive processes of repair can become maladaptive. These mechanisms, which include G2/M cell-cycle arrest, cell senescence, profibrogenic cytokine production, and activation of pericytes and interstitial myofibroblasts, contribute to the development of progressive fibrotic kidney disease. The end result is a state that mimics accelerated kidney ageing. These mechanisms present important opportunities for the design of targeted therapeutic strategies to promote adaptive renal recovery and minimize progressive fibrosis and chronic kidney disease after acute insults.

Subfields: Nephrology

View Paper: https://www.semanticscholar.org/paper/24af52875f017bfcf5d69624306274a7a77a1a0b

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Citations in the corpus

• Renal tubule injury: a driving force toward chronic kidney disease. (2018, background): “Thus, targeting the G2/M and G1/S checkpoints may be an attractive therapeutic strategy to prevent progressive CKD.145,146,211 Interestingly, the induction of a transient G0/G1 arrest in TECs before ischemia/reperfusion injury is able to ameliorate kidney injury by preventing apoptosis and profibrot”