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Cellular pathophysiology of ischemic acute kidney injury
Joseph V. Bonventre, Li Yang
Joseph V. Bonventre, Li Yang
Published November 1, 2011
Citation Information: J Clin Invest. 2011;121(11):4210-4221. https://doi.org/10.1172/JCI45161.
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Science in Medicine

Cellular pathophysiology of ischemic acute kidney injury

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Abstract

Ischemic kidney injury often occurs in the context of multiple organ failure and sepsis. Here, we review the major components of this dynamic process, which involves hemodynamic alterations, inflammation, and endothelial and epithelial cell injury, followed by repair that can be adaptive and restore epithelial integrity or maladaptive, leading to chronic kidney disease. Better understanding of the cellular pathophysiological processes underlying kidney injury and repair will hopefully result in the design of more targeted therapies to prevent the injury, hasten repair, and minimize chronic progressive kidney disease.

Authors

Joseph V. Bonventre, Li Yang

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Figure 7

Abnormal repair in ischemic AKI.

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Abnormal repair in ischemic AKI.
Repair after AKI can result in incomple...
Repair after AKI can result in incomplete repair and fibrotic lesions, which may result in progressive renal dysfunction. Factors including long-term hypoxia and hypertension result from chronic loss of peritubular microvessels. Sustained production of profibrotic cytokines such as IL-13, arginase, and TGF-β1 from the chronically activated macrophages (MΦ) contribute to postischemic fibrosis. Renal tubular epithelial cells also play a critical role in the development of fibrosis through fundamental changes in their proliferation processes, including cell cycle arrest in the G2/M phase. This results in a secretory phenotype that facilitates the production by the epithelial cells of profibrotic growth factors (including TGF-β1 and CTGF). Fibrogenesis is stimulated, and progression to chronic renal failure is accelerated.

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