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Published on: August 30, 2011
Renal stress response and acute renal failure
1Department of Medicine, University of Texas Medical Branch at Galveston 77555-0562, USA.
Advances in Renal Replacement Therapy
|April 1, 1997
Summary
Kidney cells react differently to injury, with some dying and others regenerating. Targeting stress-activated protein kinases (SAPKs) may improve outcomes in acute renal failure.
Area of Science:
- Nephrology
- Cell Biology
- Molecular Medicine
Background:
- Renal epithelial cells exhibit heterogeneous responses to in vivo injury, including necrosis, apoptosis, and survival.
- Injured tubules undergo repair involving DNA synthesis in new cells.
- Nephrotoxic and ischemic renal damage trigger an immediate early gene (IEG) response, not always linked to proliferation.
Purpose of the Study:
- To investigate the role of immediate early gene (IEG) response in renal injury.
- To explore the involvement of stress-activated protein kinases (SAPKs) in renal cell fate.
- To identify therapeutic targets for ameliorating acute renal failure.
Main Methods:
- Analysis of heterogeneous renal epithelial cell reactions to injury (necrosis, apoptosis, survival).
- Observation of DNA synthesis in cells relining injured tubules.
- Investigation of immediate early gene (IEG) response and its relation to proliferation.
- Examination of stress-activated protein kinases (SAPKs) in mediating cell-cycle arrest and apoptosis.
Main Results:
- Immediate early gene (IEG) response in renal damage is not consistently associated with DNA synthesis.
- Stress-activated protein kinases (SAPKs) activation can induce cell-cycle arrest and apoptosis.
- Downregulation of SAPKs improves renal function and long-term outcomes in ischemic renal failure.
Conclusions:
- Manipulation of SAPK pathways holds potential for treating acute renal failure.
- Understanding renal cell stress transduction pathways is crucial for developing targeted therapies.
- Identifying factors promoting renal cell survival can alter the course of renal failure.
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