Deficient heat shock protein expression: a potential mechanism for the sudden infant death syndrome.
Induction of heat shock proteins follows a metabolic stress and protects from subsequent stresses. Stressors proposed for the sudden infant death syndrome include infection, environmentally-induced hyperthermia and hypoxia. Failure to express heat shock proteins to such stressful conditions may lead to reduced tolerance, and enhance inappropriate physiologic responses and vulnerability which ultimately may lead to infant death.
Gozal
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Department of Pediatrics and Physiology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
D005334:Fever; D015870:Gene Expression; D006360:Heat-Shock Proteins / Q000096:biosynthesis* / Q000172:deficiency*; D006801:Humans; D000860:Hypoxia; D007223:Infant; D008954:Models, Biological; D013312:Stress, Physiological; D013398:Sudden Infant Death / Q000209:etiology*
D006360:Heat-Shock Proteins