期刊
FREE RADICAL BIOLOGY AND MEDICINE
卷 129, 期 -, 页码 155-168出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2018.09.019
关键词
Mitochondria; Redox imbalance; Aldehydes; Cardiovascular diseases; Therapy; Exercise training
资金
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [FAPESP 2012/05765-2, 2013/07937-8, 2015/20783-5, 2015/22814-5, 2017/16694-2]
- Conselho Nacional de Pesquisa e Desenvolvimento - Brasil [CNPq 303281/2015-4, 470880/2012-0, 407306/2013-7]
- National Institutes of Health [NIAAA MERIT Award] [AA011147]
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior - Brasil (CAPES) [001]
- FAPESP [2016/00900-0, 2017/14426-0]
- Fundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [15/20783-5, 15/22814-5] Funding Source: FAPESP
Mitochondrial dysfunction characterized by impaired bioenergetics, oxidative stress and aldehydic load is a hallmark of heart failure. Recently, different research groups have provided evidence that selective activation of mitochondrial detoxifying systems that counteract excessive accumulation of ROS, RNS and reactive aldehydes is sufficient to stop cardiac degeneration upon chronic stress, such as heart failure. Therefore, pharmacological and non-pharmacological approaches targeting mitochondria detoxification may play a critical role in the prevention or treatment of heart failure. In this review we discuss the most recent findings on the central role of mitochondrial dysfunction, oxidative stress and aldehydic load in heart failure, highlighting the most recent preclinical and clinical studies using mitochondria-targeted molecules and exercise training as effective tools against heart failure.
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