Abstract

Local hypothermia has protective effects on injured endothelial cells, cardiomyocytes, and neurocytes. Unfortunately, the underlying mechanism of local hypothermia is still unknown. The overall effect of local hypothermia involves changes in cellular and extracellular homeostasis. Reduction in cellular metabolism is the hallmark effect of local hypothermia, resulting in a reduction in energy expenditure already impaired by starvation conditions, such as ischemia. However, on a molecular basis, local hypothermia modifies cell physiology according to the type and the vitality of the cells (brain cells are more important than skin cells; therefore, local hypothermia of the brain tissue is more critical than skin tissue, and the overall reaction of the organism is to prevent the brain from dying). This involves activating survival mechanisms, such as autophagy of brain tissue and apoptosis. The activated signaling pathways are not identical in various tissues. However, the whole machinery signaling axes have not yet been elucidated. Local hypothermia promotes the healing of the injury and improves the proliferation of regenerative tissue, but not differentiation. Hypothermia prevents the transdifferentiation of endothelial cells, neurons, and myocardiocytes. Finally, the therapeutic effects of hypothermia involve activating the nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1).