Oxidative stress in heart failure: The role of mitochondria

Research output: Contribution to journalArticle

51 Citations (Scopus)

Abstract

Recent experimental and clinical studies have suggested that oxidative stress is enhanced in heart failure. The production of oxygen radicals is increased in the failing heart whereas antioxidant enzyme activities are preserved. Mitochondrial electron transport is an enzymatic source of oxygen radical generation and also a target against oxidant-induced damage. Chronic increases in oxygen radical production in the mitochondria can lead to a catastrophic cycle of mitochondrial DNA damage as well as functional decline, further radical generation, and cellular injury. These cellular events might play an important role in the development and progression of myocardial remodeling and failure.

Original languageEnglish
Pages (from-to)1177-1182
Number of pages6
JournalInternal Medicine
Volume40
Issue number12
DOIs
Publication statusPublished - Jan 1 2001

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Reactive Oxygen Species
Mitochondria
Oxidative Stress
Heart Failure
Electron Transport
Mitochondrial DNA
Oxidants
DNA Damage
Antioxidants
Wounds and Injuries
Enzymes
Clinical Studies

All Science Journal Classification (ASJC) codes

  • Internal Medicine

Cite this

Oxidative stress in heart failure : The role of mitochondria. / Tsutsui, Hiroyuki.

In: Internal Medicine, Vol. 40, No. 12, 01.01.2001, p. 1177-1182.

Research output: Contribution to journalArticle

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