Editorial: Emerging mechanisms in cardiovascular disease

Abstract

The leading cause of worldwide mortality is cardiovascular disease (CVD) (Aboukhater et al., 2023). Despite many significant advances in the field, CVD continues to claim more lives than all cancers combined (Sawma et al., 2022). There is then an urgent need for more efficacious treatment modalities or therapeutics that could aid in the management of CVD (Badran et al., 2019;Maaliki et al., 2019;El-Hachem et al., 2021). For such potential new drugs to be determined, a better understanding of the underlying mechanisms and the potential targets is critical. This Research Topic seeks to highlight a few of these emerging mechanisms and targets that could be employed for a better treatment of CVD.Myocardial injury continues to be a major contributor to CVD-associated mortality. In this thematic issue, Liu et al. discuss how they established a model for coronary microembolization (CME) in rats, and report that ferroptosis and inflammation are two key players in CME-induced myocardial injury. The authors then show that suppressing ferroptosis attenuates myocardial injury and inflammation following CME. It appears that Ptgs2, a core factor in ferroptosis, and Hif1a are the two mediators of this suppressed ferroptosis. Importantly, the authors further report that by inhibiting the Hif1a/Ptgs2 axis, atorvastatin was able to suppress ferroptosis-dependent CME-precipitated myocardial injury and inflammation (Liu et al.).In a longitudinal study, Cassano et al. report that in patients suffering from heart failure with reduced ejection fraction (HFrEF), sacubitril/valsartan suppressed oxidative stress, inhibited platelet activation, and improved endothelial dysfunction. These findings further support the utilization of sacubitril/valsartan in HFrEF, especially that the beneficial effects reported were noticed after 6 months of having patients on sacubitril/valsartan.The role of mitochondria in various aspects of the cardiovascular system is becoming clearer and more appreciated. In this Research Topic, Fang et al. show that mitochondrial fission is an emerging player in vascular smooth muscle cell lipid deposition and foaming. The authors also report that stimulation with oxidized low-density lipoprotein (ox-LDL) could drive over-fission, and eventually precipitating dysfunction, of mitochondria (Fang et al.). Interestingly, some natural products are being considered as agents that could reduce the burden of mitochondrial dysfunction. In this Research Topic, Liao et al. discuss how natural compounds could target mitochondrial dysfunction, and how such an approach