Impact of Exercise and Metabolic Disorders on Heat Shock Proteins and Vascular Inflammation

Figure 1

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 [1], 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 [2]. In addition, exercise activates adrenergic and shear stress intracellular signaling pathways [3]. Consequently HSF1 trimerizes and binds to heat shock elements (HSE) of nuclear DNA [4], whereupon specific phosphorylation/dephosphorylation events lead to a heat shock response [5]. Adapted from Noble, Melling, and Milne [6].