Cardiovascular diseases (CVDs), such as ischaemic heart disease, cardiomyopathy, atherosclerosis, hypertension, stroke and heart failure, are among the leading causes of morbidity and mortality worldwide. Although specific CVDs and the associated cardiometabolic abnormalities have distinct pathophysiological and clinical manifestations, they often share common traits, including disruption of proteostasis resulting in accumulation of unfolded or misfolded proteins in the endoplasmic reticulum (ER). ER proteostasis is governed by the unfolded protein response (UPR), a signalling pathway that adjusts the protein-folding capacity of the cell to sustain the cell’s secretory function. When the adaptive UPR fails to preserve ER homeostasis, a maladaptive or terminal UPR is engaged, leading to the disruption of ER integrity and to apoptosis. ER stress functions as a double-edged sword, with long-term ER stress resulting in cellular defects causing disturbed cardiovascular function. In this Review, we discuss the distinct roles of the UPR and ER stress response as both causes and consequences of CVD. We also summarize the latest advances in our understanding of the importance of the UPR and ER stress in the pathogenesis of CVD and discuss potential therapeutic strategies aimed at restoring ER proteostasis in CVDs. In this Review, Ren and colleagues summarize the latest advances in understanding the unfolded protein response and endoplasmic reticulum stress in the pathogenesis of cardiovascular disease and discuss potential therapeutic strategies aimed at restoring endoplasmic reticulum proteostasis in cardiovascular diseases.

Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases.

Mitophagy and mitochondrial integrity in cardiac ischemia-reperfusion injury.

Pomegranate (Punica granatum L.), one of the oldest known edible fruits, is nowadays broadly consumed throughout the world. Its fruits and seeds as well as other anatomical compartments (e.g., flowers and leaves) are rich in numerous bioactive compounds and therefore, the scientific interest in this plant has been constantly growing in recent years. It has been shown that pomegranate and its extracts exhibit potent antioxidative, antimicrobial, and anticarcinogenic properties. The present review summarizes some recent studies on pomegranate, highlighting mainly its vasculoprotective role attributed to the presence of hydrolyzable tannins ellagitannins and ellagic acid, as well as other compounds (e.g., anthocyanins and flavonoids). These in vitro and in vivo studies showed that substances derived from pomegranate reduce oxidative stress and platelet aggregation, diminish lipid uptake by macrophages, positively influence endothelial cell function, and are involved in blood pressure regulation. Clinical studies demonstrated that daily intake of pomegranate juice lessens hypertension and attenuates atherosclerosis in humans. Altogether, the reviewed studies point out the potential benefits of a broader use of pomegranate and its constituents as dietary supplements or as adjuvants in therapy of vascular diseases, such as hypertension, coronary artery disease, and peripheral artery disease.

Vasculoprotective Effects of Pomegranate (Punica granatum L.).

Impact of the Natural Compound Urolithin A on Health, Disease, and Aging

Hesperidin belongs to flavanones class of flavonoids and is known to possess broad-spectrum applicability to prevent dreadful diseases such as cardiovascular disease, neurodegeneration, and cancer....

Molecular mechanisms of action of hesperidin in cancer: Recent trends and advancements.

Urolithin A alleviates myocardial ischemia/reperfusion injury via PI3K/Akt pathway.

Liraglutide relieves myocardial damage by promoting autophagy via AMPK-mTOR signaling pathway in zucker diabetic fatty rat.

Gastrodin pretreatment alleviates myocardial ischemia/reperfusion injury through promoting autophagic flux.

Sulforaphane prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating SIRT1 and subsequently inhibiting ER stress

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Lu Tang

Papers

Urolithin A alleviates myocardial ischemia/reperfusion injury via PI3K/Akt pathway.

Liraglutide relieves myocardial damage by promoting autophagy via AMPK-mTOR signaling pathway in zucker diabetic fatty rat.

Gastrodin pretreatment alleviates myocardial ischemia/reperfusion injury through promoting autophagic flux.

Sulforaphane prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating SIRT1 and subsequently inhibiting ER stress.

Hesperetin post-treatment prevents rat cardiomyocytes from hypoxia/reoxygenation injury in vitro via activating PI3K/Akt signaling pathway