Mitochondrial oxidative stress and heart failure

研究成果: ジャーナルへの寄稿評論記事

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Recent experimental and clinical studies have suggested that oxidative stress is enhanced in heart failure. Chronic increases in oxygen radical production in the mitochondria can lead to a catastrophic cycle of mitochondrial DNA (mtDNA) damage as well as functional decline, further oxygen radical generation, and cellular injury. Reactive oxygen species induce myocyte hypertrophy, apoptosis, and interstitial fibrosis by activating matrix metalloproteinases. These cellular events play an important role in the development and progression of maladaptive cardiac remodeling and failure. Overexpression of mitchondrial transcription factor A (TFAM) could ameliorate the decline in mtDNA copy number and preserve it at a normal level in failing hearts. Consistent with alterations in mtDNA, the decrease in oxidative capacities was also prevented. Therefore, the activation of TFAM expression could ameliorate the pathophysiological process seen in myocardial failure. Inhibition of mitochondrial oxidative stress and DNA damage could be the most effective and novel treatment strategies for heart failure.

元の言語英語
ページ(範囲)809-813
ページ数5
ジャーナルInternal Medicine
45
発行部数13
DOI
出版物ステータス出版済み - 8 1 2006
外部発表Yes

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All Science Journal Classification (ASJC) codes

  • Internal Medicine

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