ABSTRACT
Acute renal failure (ARF) in humans is caused by either ischemia and reperfusion (IR) or nephrotoxic chemicals, and the proximal tubular epithelium is generally the primary target. Extensive research on molecular mechanisms of acute renal tubular pathologies has led to improved insight into the molecular and cellular mechanisms of renal cell injury. Despite these efforts, ARF still remains an important clinical problem. Therefore, further basic research to better understand the molecular basis of renal cell injury and repair remains crucial for identifying potential novel therapeutic strategies, either to combat the initiation phase of ARF or to accelerate the renal regeneration process. Such strategies may interfere with any of the phases that can be recognized in the ARF and regeneration process: (sublethal) injury of proximal tubular epithelial cells, initiation of cellular repair, survival or death programs, and regeneration of damaged tubules by increased proliferation followed by differentiation.
