Cell cycle regulation: repair and regeneration in acute renal failure.
Research into mechanisms of acute renal failure has begun to reveal molecular targets for possible therapeutic intervention. Much useful knowledge into the causes and prevention of this syndrome has been gained by the study of animal models. Most recently, investigation of the effects on acute renal failure of selected gene knock-outs in mice has contributed to our recognition of many previously unappreciated molecular pathways. Particularly, experiments have revealed the protective nature of two highly induced genes whose functions are to inhibit and control the cell cycle after acute renal failure. By use of these models we have started to understand the role of increased cell cycle activity after renal stress, and the role of proteins induced by these stresses that limit this proliferation.
Price
Peter M
PM
Department of Internal Medicine, University of Arkansas for Medical Sciences and Department of Veterans Affairs Medical Center, Little Rock, Arkansas 72205, USA. PricePeter@uams.edu
Megyesi
Judit
J
Saf Irstein
Robert L
RL
D058186:Acute Kidney Injury / Q000378:metabolism* / Q000473:pathology*; D000818:Animals; D018797:Cell Cycle Proteins / Q000378:metabolism*; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins / Q000378:metabolism*; D006801:Humans; D007668:Kidney / Q000378:metabolism / Q000473:pathology
C493956:CDKN1A protein, human; D018797:Cell Cycle Proteins; D050759:Cyclin-Dependent Kinase Inhibitor p21; D016213:Cyclins