CNC-Center for Neuroscience and Cell Biology, UC-Biotech, University of Coimbra, Biocant Park, Cantanhede, Portugal.
Clinica Medica "A. Murri", Department of Biomedical Sciences and Human Oncology, University of Bari "Aldo Moro" Medical School, Bari, Italy.
Curr Pharm Des. 2019;25(29):3175-3194. doi: 10.2174/1389203720666190830163735.
Cardiovascular diseases (CVDs) are a leading risk factor for mortality worldwide and the number of CVDs victims is predicted to rise through 2030. While several external parameters (genetic, behavioral, environmental and physiological) contribute to cardiovascular morbidity and mortality; intrinsic metabolic and functional determinants such as insulin resistance, hyperglycemia, inflammation, high blood pressure and dyslipidemia are considered to be dominant factors.
Pubmed searches were performed using different keywords related with mitochondria and cardiovascular disease and risk. In vitro, animal and human results were extracted from the hits obtained.
High cardiac energy demand is sustained by mitochondrial ATP production, and abnormal mitochondrial function has been associated with several lifestyle- and aging-related pathologies in the developed world such as diabetes, non-alcoholic fatty liver disease (NAFLD) and kidney diseases, that in turn can lead to cardiac injury. In order to delay cardiac mitochondrial dysfunction in the context of cardiovascular risk, regular physical activity has been shown to improve mitochondrial parameters and myocardial tolerance to ischemia-reperfusion (IR). Furthermore, pharmacological interventions can prevent the risk of CVDs. Therapeutic agents that can target mitochondria, decreasing ROS production and improve its function have been intensively researched. One example is the mitochondria-targeted antioxidant MitoQ10, which already showed beneficial effects in hypertensive rat models. Carvedilol or antidiabetic drugs also showed protective effects by preventing cardiac mitochondrial oxidative damage.
This review highlights the role of mitochondrial dysfunction in CVDs, also show-casing several approaches that act by improving mitochondrial function in the heart, contributing to decrease some of the risk factors associated with CVDs.
心血管疾病（CVDs）是全球范围内导致死亡的主要风险因素，预计到 2030 年 CVDs 患者人数将上升。虽然一些外部参数（遗传、行为、环境和生理）导致心血管发病率和死亡率增加，但内在的代谢和功能决定因素，如胰岛素抵抗、高血糖、炎症、高血压和血脂异常，被认为是主要因素。
使用与线粒体和心血管疾病及风险相关的不同关键词在 Pubmed 上进行检索，并从获得的命中中提取体外、动物和人体结果。
高心脏能量需求由线粒体 ATP 产生来维持，异常的线粒体功能与发达国家的几种与生活方式和衰老相关的病理学有关，如糖尿病、非酒精性脂肪肝（NAFLD）和肾脏疾病，而这些疾病反过来又会导致心脏损伤。为了在心血管风险的情况下延缓心脏线粒体功能障碍，有规律的体育活动已被证明可以改善线粒体参数和心肌对缺血再灌注（IR）的耐受性。此外，药物干预可以预防 CVDs 的风险。已经对能够靶向线粒体、减少 ROS 产生并改善其功能的治疗药物进行了深入研究。一个例子是靶向线粒体的抗氧化剂 MitoQ10，它已在高血压大鼠模型中显示出有益的效果。卡维地洛或抗糖尿病药物也通过防止心脏线粒体氧化损伤显示出保护作用。
本文综述了线粒体功能障碍在 CVDs 中的作用，同时展示了几种通过改善心脏中线粒体功能来降低与 CVDs 相关的一些风险因素的方法。
