Mitochondrial cardiovascular diseases: molecular mechanisms, multi-omics exploration and therapeutic strategies

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Background Recent research highlights that abnormal mitochondrial function is a key feature in several cardiovascular diseases (CVDs), including aortic dissection, aortic aneurysm, atherosclerosis, pulmonary hypertension, and heart failure. We propose a novel concept termed mitochondrial cardiovascular diseases (Mito-CVDs) to define these conditions, which involve heart and vascular disorders directly driven by mitochondrial impairments, with the aim of highlighting the critical role of mitochondria in CVDs. Aim of review This review aims to explore the complex relationship between mitochondrial impairments and Mito-CVDs, offering insights into potential molecular mechanisms and therapeutic strategies to address these diseases. Key scientific concepts of review The role of mitochondrial impairments in CVDs is expounded upon in detail, encompassing aspects such as excessive production of Reactive Oxygen Species (ROS), diminished Oxidative Phosphorylation (OXPHOS) capacity, and perturbations in Ca 2+ transport. We also recapitulate the application of mitochondrial multi-omics, incorporating genomics, transcriptomics, proteomics, and metabolomics, within the realm of CVDs research. Additionally, single-cell mtDNA sequencing technology unfolds novel vistas for disclosing mitochondrial heterogeneity and status functional in Mito-CVDs. To enhance the understanding of Mito-CVDs, we pr

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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