Exposure to extreme environmental temperatures leads to acute and chronic human health problems, such as morbidity and mortality1,2. This varies with the intensity and duration of the temperature event, the level of acclimatization, public readiness and adaptation, and the extent to which essential infrastructure and social services are affected. Sqwincher Ind

Heat stress induces a range of adaptive physiological and cellular mechanisms, including thermoregulation and the cellular stress response (CSR), with the induction of heat shock proteins (HSPs) to prevent hyperthermia and cellular damage1–3. At the vascular level, maladaptive responses to heat include cardiovascular stress, which increases cardiac output to accelerate the transport of heat from the cells to the surface, leading to heart failure and death7.

The Science of Heat Stress: How to Protect Your Body

At the cellular level, oxidative stress caused by increased generation of reactive oxygen species (ROS) compromises membrane lipids and pigments causing a loss of water and ions across cell membranes, and inhibiting mitochondrial and chloroplast functions in carbon metabolism leading to reduced energy production. The cellular redox balance can be restored by increasing HSPs to protect against heat-induced damage, and by detoxification mechanisms.

Despite these complex metabolic and signaling pathways, developing a heat-tolerant crop is challenging, as the genetic basis for tolerance remains largely unresolved. We therefore analyzed, for the first time, transcriptomes from peripheral blood mononuclear cells (PBMCs) from healthy volunteers passively exposed to short periods of severe environmental heat in a sauna with a full recovery phenotype.

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