Mitochondrial complex I deficiency and cardiovascular diseases: current evidence and future directions

被引:41
作者
Forte, Maurizio [1 ]
Palmerio, Silvia [1 ]
Bianchi, Franca [1 ]
Volpe, Massimo [1 ,2 ]
Rubattu, Speranza [1 ,2 ]
机构
[1] IRCCS Neuromed, Dept Angiocardioneurol, I-86077 Pozzilli, IS, Italy
[2] Sapienza Univ Rome, Osped S Andrea, Sch Med & Psychol, Dept Clin & Mol Med, Rome, Italy
来源
JOURNAL OF MOLECULAR MEDICINE-JMM | 2019年 / 97卷 / 05期
关键词
Mitochondrial complex I; Mitochondrial dysfunction; Cardiovascular diseases; Therapeutic interventions; Cardiac hypertrophy; Stroke; ISCHEMIA-REPERFUSION INJURY; OXIDATIVE STRESS; HEART-FAILURE; CARDIOMYOCYTE APOPTOSIS; CARDIAC-HYPERTROPHY; THERAPEUTIC TARGET; ENZYMATIC-ACTIVITY; CHAIN DYSFUNCTION; REDOX REGULATION; ASSEMBLY FACTOR;
D O I
10.1007/s00109-019-01771-3
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Compelling evidence demonstrates the emerging role of mitochondrial complex I deficiency in the onset and development of cardiovascular diseases (CVDs). In particular, defects in single subunits of mitochondrial complex I have been associated with cardiac hypertrophy, ischemia/reperfusion injury, as well as diabetic complications and stroke in pre-clinical studies. Moreover, data obtained in humans revealed that genes coding for complex I proteins were associated with different CVDs. In this review, we discuss recent experimental studies that underline the contributory role of mitochondrial complex I deficiency in the etiopathogenesis of several CVDs, with a particular focus on those involving loss of function models of mitochondrial complex I. We also discuss human studies and potential therapeutic strategies able to rescue mitochondrial function in CVDs.
引用
收藏
页码:579 / 591
页数:13
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