Oxidative stress and heart failure

研究成果: Contribution to journalReview article査読

5 被引用数 (Scopus)

抄録

The excessive reactive oxygen species (ROS), produced by the electron leak in mitochondria of failing myocardium, play an important role in development and progression of heart failure (HF) and cardiac remodeling, which is associated with induction of myocyte hypertrophy and apoptosis and activation of matrix metalloproteinases. Furthermore, ROS can damage mitochondrial DNA(mtDNA), and thus lead to mitochondrial dysfunction and additional ROS generation. Recently, we found that the overexpression of mitochondrial transcription factor A (TFAM), which is essential for mtDNA transcription and replication, ameliorates cardiac remodeling and failure. Therefore, the regulation of mitochondrial oxidative stress or manipulation of TFAM protein may provide a novel therapeutic strategy of HF.

本文言語英語
ページ(範囲)848-853
ページ数6
ジャーナルNippon rinsho. Japanese journal of clinical medicine
64
5
出版ステータス出版済み - 5 2006

All Science Journal Classification (ASJC) codes

  • 医学(全般)

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