期刊
AMERICAN JOURNAL OF THE MEDICAL SCIENCES
卷 342, 期 2, 页码 120-124出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MAJ.0b013e3182249fcd
关键词
Antioxidant enzymes; Vitamin E; Alpha-to-copherol; Nitric oxide synthase; Myocardial remodeling
资金
- NHLBI NIH HHS [K08 HL003878-05, U01 HL100398, U01 HL100398-01, T32 HL007411, T32 HL007411-31, U01 HL100398-02] Funding Source: Medline
Over the past several decades, investigations in humans and animal models of heart failure (HF) have provided substantial evidence that oxidative stress is increased in HF and contributes to disease progression. The high metabolic activity of cardiac myocytes makes these cells active sources of reactive oxygen species. Work in cell and animal models clearly demonstrates that oxidative stress activates processes such as changes in gene expression and cell death that are now accepted components of myocardial remodeling and HF. Antioxidants prevent progressive remodeling and even improve cardiac function in animal models of HF. It is therefore disappointing that to date no antioxidant strategy has translated to a therapeutic in the HF clinic. Possible explanations, including inadequate appreciation of the critical disease-modifying sources of reactive oxygen species, the choice of the wrong antioxidant strategy, or incomplete understanding of individual variability in human antioxidant defenses in this brief review.
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