Rescue of Heart Failure by Mitochondrial Recovery

被引:8
|
作者
Marquez, Jubert [1 ]
Lee, Sung Ryul [1 ]
Kim, Nari [1 ]
Han, Jin [1 ]
机构
[1] Inje Univ, Natl Res Lab Mitochondrial Signaling, Dept Hlth Sci & Technol,Project Team BK21, Cardiovasc & Metab Dis Ctr,Coll Med,Dept Physiol, 75 Bokji Ro, Busan 47392, South Korea
基金
新加坡国家研究基金会;
关键词
Mitochondria; Heart Failure; Oxidative Stress; Protein Processing; Post-Translational; Mitochondrial Permeability Transition Pore; PERMEABILITY TRANSITION PORE; NITRIC-OXIDE SYNTHASE; PRESSURE-OVERLOAD; CYCLOPHILIN-D; POSTTRANSLATIONAL MODIFICATIONS; CARDIOVASCULAR-DISEASE; DILATED CARDIOMYOPATHY; INDUCED HYPERTROPHY; REPERFUSION INJURY; CARDIAC RESPONSE;
D O I
10.5213/inj.1632570.285
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Heart failure (HF) is a multifactorial disease brought about by numerous, and oftentimes complex, etiological mechanisms. Although well studied, HF continues to affect millions of people worldwide and current treatments can only prevent further progression of HF. Mitochondria undoubtedly play an important role in the progression of HF, and numerous studies have highlighted mitochondrial components that contribute to HF. This review presents an overview of the role of mitochondrial biogenesis, mitochondrial oxidative stress, and mitochondrial permeability transition pore in HF, discusses ongoing studies that attempt to address the disease through mitochondrial targeting, and provides an insight on how these studies can affect future research on HF treatment.
引用
收藏
页码:5 / 12
页数:8
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