The mitochondria are essential organelles that generate large amounts of ATP via the electron transport chain (ECT). Mitochondrial dysfunction causes reactive oxygen species accumulation, energy stress, and cell death. Endothelial mitochondrial dysfunction is an important factor causing abnormal function of the endothelium, which plays a central role during atherosclerosis development. Atherosclerosis-related risk factors, including high glucose levels, hypertension, ischemia, hypoxia, and diabetes, promote mitochondrial dysfunction in endothelial cells. This review summarizes the physiological and pathophysiological roles of endothelial mitochondria in endothelial function and atherosclerosis.

Quercetin is one of the most common flavonoids. More and more studies have found that quercetin has great potential utilization value in cardiovascular diseases (CVD), such as antioxidant, antiplatelet aggregation, antibacterial, cholesterol lowering, endothelial cell protection, etc. However, the medicinal value of quercetin is mostly limited to animal models and preclinical studies. Due to the complexity of the human body and functional structure compared to animals, more research is needed to explore whether quercetin has the same mechanism of action and pharmacological value as animal experiments. In order to systematically understand the clinical application value of quercetin, this article reviews the research progress of quercetin in CVD, including preclinical and clinical studies. We will focus on the relationship between quercetin and common CVD, such as atherosclerosis, myocardial infarction, ischemia reperfusion injury, heart failure, hypertension and arrhythmia, etc. By elaborating on the pathophysiological mechanism and clinical application research progress of quercetin's protective effect on CVD, data support is provided for the transformation of quercetin from laboratory to clinical application.

Iron is indispensable in numerous biologic processes, but abnormal iron regulation and accumulation is related to pathological processes in cardiovascular diseases. However, the underlying mechanisms still need to be further explored. Iron plays a key role in metal‐catalyzed oxidative reactions that generate reactive oxygen species (ROS), which can cause oxidative stress. As the center for oxygen and iron utilization, mitochondria are vulnerable to damage from iron‐induced oxidative stress and participate in processes involved in iron‐related damage in cardiovascular disease, although the mechanism remains unclear. In this review, the pathological roles of iron‐related oxidative stress in cardiovascular diseases are summarized, and the potential effects and mechanisms of mitochondrial iron homeostasis and dysfunction in these diseases are especially highlighted.

Pulmonary arterial hypertension (PAH) is characterized by the increased pulmonary vascular resistance due to pulmonary vasoconstriction and vascular remodeling. PAH has high disability, high mortality and poor prognosis, which is becoming a more common global health issue. There is currently no drug that can permanently cure PAH patients. The pathogenesis of PAH is still not fully elucidated. However, the role of metabolic theory in the pathogenesis of PAH is becoming clearer, especially mitochondrial metabolism. With the deepening of mitochondrial researches in recent years, more and more studies have shown that the occurrence and development of PAH are closely related to mitochondrial dysfunction, including the tricarboxylic acid cycle, redox homeostasis, enhanced glycolysis, and increased reactive oxygen species production, calcium dysregulation, mitophagy, etc. This review will further elucidate the relationship between mitochondrial metabolism and pulmonary vasoconstriction and pulmonary vascular remodeling. It might be possible to explore more comprehensive and specific treatment strategies for PAH by understanding these mitochondrial metabolic mechanisms.