Proteotoxic stress response in atherosclerotic cardiovascular disease: Emerging role of heat shock factor 1

Atherosclerosis is a major risk factor for cardiovascular diseases. Hypercholesterolemia has been both clinically and experimentally linked to cardiovascular disease and is involved in the initiation of atherosclerosis. Heat shock factor 1 (HSF1) is involved in the control of atherosclerosis. HSF1 is a critical transcriptional factor of the proteotoxic stress response that regulates the production of heat shock proteins (HSPs) and other important activities such as lipid metabolism. Recently, HSF1 is reported to directly interact with and inhibit AMP-activated protein kinase (AMPK) to promote lipogenesis and cholesterol synthesis. This review highlights roles of HSF1 and HSPs in critical metabolic pathways of atherosclerosis, including lipogenesis and proteome homeostasis.

Automated summary

Atherosclerosis is a major risk factor for cardiovascular diseases, and hypercholesterolemia is involved in its initiation. Heat shock factor 1 (HSF1) plays a critical role in controlling atherosclerosis by regulating heat shock proteins (HSPs) and lipid metabolism. Recent research shows that HSF1 directly interacts with and inhibits AMP-activated protein kinase (AMPK), promoting lipogenesis and cholesterol synthesis. This review highlights the roles of HSF1 and HSPs in critical metabolic pathways of atherosclerosis.