Oxidative stress and heart failure

Research output: Contribution to journalReview article

5 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)848-853
Number of pages6
JournalNippon rinsho. Japanese journal of clinical medicine
Volume64
Issue number5
Publication statusPublished - May 2006
Externally publishedYes

All Science Journal Classification (ASJC) codes

  • Medicine(all)

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