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HSF and Heart Diseases

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Abstract

In the heart, HSF1 has a wide range of expression in many kinds of cells, including cardiac myocytes, fibroblasts, and endothelial cells, which governs the activation of heat shock proteins and plays a protective role against different pathological stimuli. HSF1 is activated by phosphorylation and transferred into the nucleus. HSPs also regulate HSF1 activity. HSF1 activity is required to maintain redox state and attenuate oxidative damage in the heart under normal physiological conditions. HSF1 protects against ischemia/reperfusion injury and myocardial infarction by inhibiting oxidative stress and cardiomyocyte apoptosis. HSF1 ameliorated death of cardiomyocytes and cardiac fibrosis and thereby prevented cardiac dysfunction as well as hypertrophy induced by chronic pressure overload. HSF1 promotes cardiac angiogenesis during chronic pressure overload, leading to the maintenance of cardiac adaptation. In atherosclerosis, however, HSF1 is activated and highly expressed in atherosclerotic lesions and that proinflammatory cytokine stimulation and disturbed mechanical stress to the vessel are primarily responsible for HSF1 activation in smooth muscle cells. In the failing hearts, HSF1 is increased, but nuclear translocation of the HSF1 is markedly reduced in the viable myocardium upon the pathological stresses. Thus, cardiac protective HSP induction is impaired in the failing heart.

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Yuan, J., Zou, Y. (2016). HSF and Heart Diseases. In: Nakai, A. (eds) Heat Shock Factor. Springer, Tokyo. https://doi.org/10.1007/978-4-431-55852-1_12

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