Laboratory of Environmental Physiology, Faculty of Dental Medicine, The Hebrew University, Jerusalem, Israel.
Ann N Y Acad Sci. 2010 Feb;1188:199-206. doi: 10.1111/j.1749-6632.2009.05101.x.
Heat acclimation (AC) is an evolutionarily conserved feature allowing adjustment to persistent changes in ambient temperature. The mechanisms underlying acclimation involve a continuum of physiologic changes, determined by temperature-adaptive shifts in gene expression. The AC heart generates greater pressure at lower O2 consumption, but at the expense of contractile velocity, and renders cytoprotection to a wide range of stressors (cross-tolerance) via greater cytoprotective protein reserves, faster post-injury molecular dynamic response, and post-translational modifications. A greater abundance of HSP70 and HIF-1alpha and its metabolic targeted genes (both nuclear and mitochondrial) are among the cytoprotective changes that occur. The cytoprotection profile provides a dual protective strategy--a constitutive availability of cytoprotective proteins without a need for de novo protein synthesis, together with an "alerted system" responding rapidly upon insult. Hence, cross-tolerance is achieved via activation of "on-call" constitutive cytoprotection shared by all stressors, together with organ-specific functional remodeling and stress-specific cross-talk.
热适应(AC)是一种进化保守的特征,允许对环境温度的持续变化进行调整。适应的机制涉及一系列生理变化,由基因表达的温度适应性变化决定。AC 心脏在较低的耗氧量下产生更大的压力,但代价是收缩速度,并且通过更多的细胞保护蛋白储备、更快的损伤后分子动态反应和翻译后修饰来对广泛的应激源(交叉耐受)产生细胞保护作用。热休克蛋白 70(HSP70)和缺氧诱导因子 1α(HIF-1α)及其代谢靶向基因(核和线粒体)的丰度增加是发生的细胞保护变化之一。细胞保护谱提供了一种双重保护策略——无需新的蛋白质合成即可提供持续的细胞保护蛋白,同时还具有一种“警报系统”,在受到伤害时迅速做出反应。因此,通过激活所有应激源共有的“待命”组成型细胞保护作用,以及器官特异性功能重塑和应激特异性交叉对话,实现了交叉耐受。