Abstract
In different pathological states that cause endoplasmic reticulum (ER) calcium depletion, altered glycosylation, nutrient deprivation, oxidative stress, DNA damage or energy perturbation/fluctuations, the protein folding process is disrupted and the ER becomes stressed. Studies in the past decade have demonstrated that ER stress is closely associated with pathogenesis of obesity, insulin resistance and type 2 diabetes. Excess nutrients and inflammatory cytokines associated with metabolic diseases can trigger or worsen ER stress. ER stress plays a critical role in the induction of endothelial dysfunction and atherosclerosis. Signaling pathways including AMP-activated protein kinase and peroxisome proliferator-activated receptor have been identified to regulate ER stress, whilst ER stress contributes to the imbalanced production between nitric oxide (NO) and reactive oxygen species (ROS) causing oxidative stress. Several drugs or herbs have been proved to protect against cardiovascular diseases (CVD) through inhibition of ER stress and oxidative stress. The present article reviews the involvement of ER stress and oxidative stress in cardiovascular dysfunction and the potential therapeutic implications.
Highlights
endoplasmic reticulum (ER) stress markers PKR-like ER kinase (PERK), IRE1α, ATF6α and Jun N-terminal kinase (JNK) are activated in obese mice and in mice fed a high-fat diet [59,60]
Research targeting ER stress in Pulmonary arterial hypertension (PAH) has focused on pulmonary artery smooth muscle cells (PASMC), as exaggerated proliferation and resistance to apoptosis of PASMCs is a key component of vascular remodeling [126]
All this evidence supports the interaction among ER stress, oxidative stress and inflammation contributing to myocardial infarction (MI) and the potential therapeutic implications such as using valsartan, natural plants (PN-F) and exercise
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. UPS and ER jointly maintain cell homeostasis and participate in the major pathways of signal transduction, cell cycle regulation and Antioxidants 2021, 10, 1167. Oxidative stress is mainly caused by imbalanced production of reactive oxygen species (ROS) and antioxidants [9,10]. The low concentrations of ROS play an important role in cell homeostasis by regulating cell signal transduction and physiological activity [13]. When the production of ROS exceeds the control of the antioxidant defense mechanisms, oxidative stress will occur, hindering protein folding, damaging the synthesis and accumulating toxic products, which affect the normal function of cells and lead to cell death, and may lead to diseases in the cardiovascular system [9,14,15,16]. The present article reviews the involvement of ER stress and oxidative stress in cardiovascular dysfunction and the potential therapeutic implications
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