Mitochondrial oxidative stress and heart failure

Research output: Contribution to journalReview article

42 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)809-813
Number of pages5
JournalInternal Medicine
Volume45
Issue number13
DOIs
Publication statusPublished - Aug 1 2006
Externally publishedYes

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Oxidative Stress
Heart Failure
Mitochondrial DNA
Reactive Oxygen Species
DNA Damage
Matrix Metalloproteinases
Muscle Cells
Hypertrophy
Mitochondria
Fibrosis
Transcription Factors
Apoptosis
Wounds and Injuries

All Science Journal Classification (ASJC) codes

  • Internal Medicine

Cite this

Mitochondrial oxidative stress and heart failure. / Tsutsui, Hiroyuki.

In: Internal Medicine, Vol. 45, No. 13, 01.08.2006, p. 809-813.

Research output: Contribution to journalReview article

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