Is stress response a new link between adipose tissue and atherogenesis? The role of HSPs/HSF1

This editorial refers to ‘Heat shock factor-1 knockout enhances cholesterol 7α-hydroxylase (CYP7A1) and multidrug transporter (MDR1) gene expressions to attenuate atherosclerosis’, by K. Krishnamurthy et al. , pp. 74–83. The role of lipids in atherogenesis is well established; subendothelial deposition of oxidized low-density lipoprotein (ox-LDL) initiates atherosclerotic plaque formation.1 Circulating cholesterol is regulated by its dietary intake and endogenous synthesis on one hand, and its elimination from the circulation via LDL-receptors/excretion in the bile on the other hand.2 Various lipid-lowering therapies targeting these regulatory mechanisms are used in patients with dyslipidaemias, significantly impacting cardiovascular risk. However, the residual risk after applying existing lipid-lowering strategies highlights the complexity of lipid metabolism and the necessity for broader understanding of the links between lipids and the cardiovascular system. Over the last decade, it became clear that adipose tissue is an active endocrine organ producing various adipocytokines, the secretory profile of which is dysregulated in cardiovascular and metabolic disease. Adipocyte differentiation, a process whereby small pre-adipocytes with little lipid content transform into large, differentiated lipid-rich adipocytes, is altered in cardiometabolic disease.3 Obesity-related diseases are characterized by adipose inflammatory infiltration, which prevents pre-adipocyte differentiation, affecting lipid and energy consumption/expenditure and modifying the secretory profile of the tissue.3 The literature on the roles …