Impact of Exercise and Metabolic Disorders on Heat Shock Proteins and Vascular Inflammation
Schematic representation of activation of HSF1 with exercise and accompanying increases in vascular stress. Exercise initiates a number of factors, including elevations in temperature, reactive oxygen species (ROS), intracellular calcium (Ca2+), and decreased energy status , which may result in intracellular protein modification leading to dissociation of the heat shock transcription factor (HSF1) and heat shock proteins Hsp in the cytoplasm . In addition, exercise activates adrenergic and shear stress intracellular signaling pathways . Consequently HSF1 trimerizes and binds to heat shock elements (HSE) of nuclear DNA , whereupon specific phosphorylation/dephosphorylation events lead to a heat shock response . Adapted from Noble, Melling, and Milne .