Gozal D
Department of Pediatrics and Physiology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Med Hypotheses. 1996 Jan;46(1):52-4. doi: 10.1016/s0306-9877(96)90236-4.
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.
热休克蛋白的诱导发生在代谢应激之后，并能保护机体免受后续应激的影响。提出的与婴儿猝死综合征相关的应激源包括感染、环境诱导的体温过高和缺氧。在这些应激条件下未能表达热休克蛋白可能会导致耐受性降低，并增强不适当的生理反应和易损性，最终可能导致婴儿死亡。
