Increased Endoplasmic Reticulum Stress in Atherosclerotic Plaques Associated With Acute Coronary Syndrome

Induction of the unfolded protein response after monocyte to macrophage differentiation augments cell survival in early atherosclerotic lesions

“…GRP78 up-regulation has a direct cytoprotective advantage against ER stress-inducing agents in the macrophage. These data, combined with previous reports indicating that ER stress occurs in the atherosclerotic lesions of animal models (9, 15) and human subjects exhibiting acute coronary syndrome (23,67), make it highly plausible that UPR induction due to macrophage differentiation influences early lesion development. Given our findings, therapeutic approaches that modulate UPR activation, including 4-phenylbutyric acid treatment (68), have the potential to influence atherosclerotic lesion development and plaque stability.…”

Endoplasmic reticulum stress: a novel mechanism and therapeutic target for cardiovascular diseases

“…Generally, in the case of mild ERS, the UPR is responsible for activating molecular chaperones to attenuate cellular dysfunction or damage. However, if ERS is prolonged or too severe, the UPR may result in the activation of apoptosis [77] . SMCs synthesize most of the inter- [78] .…”

Endoplasmic reticulum stress inhibition reduces hypertension through the preservation of resistance blood vessel structure and function

“…Endoplasmic reticulum stress occurs when misfolded proteins accumulate in the endoplasmic reticulum, which can occur in diseased blood vessels [15,16]. Importantly, oxidative processes within the blood vessels may be responsible for reduced nitric oxide bioavailability [17] and generating peroxynitrite, an endoplasmic reticulum stress inducer [16].…”