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Nephrol Dial Transplant (2000) 15: 141-144
© 2000 European Renal Association-European Dialysis and Transplant Association

Editorial Comments

Calcium-mediated proximal tubular injury—what is the role of cysteine proteases?

Charles L. Edelstein

Division of Renal Diseases and Hypertension, University of Colorado Health Sciences Center, Denver, CO, USA

Correspondence and offprint requests to: Division of Renal Diseases and Hypertension, University of Colorado Health Sciences Center, 4200 East Ninth Ave, Box C281, Denver, CO 80262, USA.

Calcium

Numerous studies over the past 15 years in different injury models and cell types have demonstrated an increase in cytosolic calcium in renal epithelial cell injury. Some of these studies are summarized in Table 1Go. However, despite these studies, crucial questions to implicate calcium as the primary factor in cell injury have remained. Does the increase in calcium precede the injury? Does preventing the rise in cytosolic calcium attenuate the injury? Recent studies have provided insight into these questions. Both Weinberg et al. [1] and Kribben et al. [2] conclusively demonstrated in proximal tubules that hypoxia is associated with a rise in cytosolic calcium which precedes any evidence of membrane damage. To further support a pathogenetic role of intracellular calcium, calcium-mediated injury is also reversible with reoxygenation [2], a calcium chelator to lower intracellular calcium [2] and by lowering . . . [Full Text of this Article]

Cysteine proteases

Role of calpain in hypoxic proximal tubular injury

Role of caspases in hypoxic proximal tubular injury

Interaction between calpain and caspases

Targets of caspases during hypoxic/ischaemic proximal tubular injury

Conclusion

References


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