[ER stress and cardiometabolic disease: role of adipokines]

ER stress is defined as an imbalance between protein synthesis and protein folding capacity, resulting in the accumulation of misfolded or unfolded protein in ER. Temperate ER stress through UPR enhances the folding capacity of ER and restores the ER homeostasis, exerting a cell protection role. While prolonged ER stress lead to inflammation, cell dysfunction and apoptosis, which takes part in the progression of insulin resistance and atherosclerosis. In the condition of obesity or hyperhomocysteinemia, ER stress in adipose tissue, hypothalamus, liver and other tissue or organs causes the dysregulation of adipokines secretion as well as abnormal receptor or post-receptor signal transduction, which plays an significant role in cardiometabolic disease.