Biology of ischemic and toxic renal tubular cell injury: role of nitric oxide and the inflammatory response.
Acute ischemic or toxic injury to the kidney induces alterations in the expression of many genes. Some of these molecular responses have been termed 'maladaptive' because they exacerbate the tubular damage induced by the initiating insult. Some maladaptive responses include alterations in the activity of nitric oxide synthases and expression of cytokines and adhesion molecules that mediate an inflammatory response. This review focuses on the role of nitric oxide and inflammation in influencing the course of acute renal failure due to ischemic and toxic tubular injury.
Lieberthal
W
W
Evans Department of Clinical Research, Boston Medical Center, Boston University Medical School, Massachusetts, USA.
D058186:Acute Kidney Injury / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D000818:Animals; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology; D007511:Ischemia / Q000503:physiopathology; D007684:Kidney Tubules / Q000098:blood supply / Q000293:injuries* / Q000503:physiopathology; D007962:Leukocytes / Q000502:physiology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000502:physiology; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; D013601:T-Lymphocytes / Q000502:physiology; D000521:alpha-MSH / Q000627:therapeutic use
D009569:Nitric Oxide; D000521:alpha-MSH; C496319:NOS2 protein, human; C496314:NOS3 protein, human; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III