National Institute on Aging (NIA), National Institutes of Health (NIH), Baltimore, Maryland.
J Gerontol A Biol Sci Med Sci. 2021 Jan 18;76(2):361-367. doi: 10.1093/gerona/glaa297.
Although mitochondrial dysfunction appears to be a contributing factor in the pathogenesis of cardiovascular and metabolic diseases, empirical data on this association are still lacking. This study evaluated whether mitochondrial oxidative capacity, as assessed by phosphorus magnetic resonance spectroscopy, was associated with cardiovascular risk, as estimated by the Framingham Risk Score (FRS), and with a clinical history of cardiovascular disease (CVD), in community-dwelling adults.
A total of 616 subjects from the Baltimore Longitudinal Study of Aging (mean age 66 years) underwent a comprehensive clinical evaluation. Mitochondrial oxidative capacity in skeletal muscle was assessed as post-exercise phosphocreatine recovery time constant by phosphorus magnetic resonance spectroscopy. Multivariate regression models were employed to determine the cross-sectional association of mitochondrial oxidative capacity with FRS and history of CVD.
Decreased mitochondrial oxidative capacity was strongly associated with higher FRS independent of age, body composition, and physical activity. Lower oxidative capacity was also associated with a history of positive of CVD and higher number of CVD events.
We speculate that the observed association could reflect the effect of an excessive production of oxidative species by dysfunctional mitochondria. Furthermore, decreased energy production could hamper the functionality of heart and vessels. In turn, a malfunctioning cardiovascular apparatus could fail to deliver the oxygen necessary for optimal mitochondrial energy production, therefore creating a vicious cycle. Longitudinal studies are necessary to ascertain the directionality of the association and the eventual presence of common pathogenetic roots. In conclusion, mitochondria could represent an important target for intervention in cardiovascular health.
尽管线粒体功能障碍似乎是心血管和代谢疾病发病机制的一个促成因素，但关于这种关联的经验数据仍然缺乏。本研究评估了通过磷磁共振波谱法评估的线粒体氧化能力是否与心血管风险（由弗雷明汉风险评分[FRS]估计）以及社区居住的成年人的心血管疾病（CVD）病史相关。
来自巴尔的摩老龄化纵向研究的 616 名受试者（平均年龄 66 岁）接受了全面的临床评估。通过磷磁共振波谱法评估骨骼肌中线粒体的氧化能力作为运动后磷酸肌酸恢复时间常数。采用多元回归模型确定线粒体氧化能力与 FRS 和 CVD 病史的横断面相关性。
与年龄、身体成分和体力活动无关，线粒体氧化能力降低与 FRS 升高密切相关。较低的氧化能力也与 CVD 病史呈阳性和 CVD 事件数量增加相关。
我们推测观察到的相关性可能反映了功能失调的线粒体产生过多氧化物质的影响。此外，能量产生减少会阻碍心脏和血管的功能。反过来，功能失调的心血管装置可能无法提供最佳线粒体能量产生所需的氧气，从而形成恶性循环。需要进行纵向研究以确定关联的方向和最终存在共同的发病根源。总之，线粒体可能是心血管健康干预的一个重要靶点。
