期刊
BIOLOGICAL CHEMISTRY
卷 389, 期 3, 页码 221-231出版社
WALTER DE GRUYTER GMBH
DOI: 10.1515/BC.2008.032
关键词
apoptosis; hormesis; longevity factor; oxidative stress; sirtuin; stress resistance
资金
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL067724, P01HL059139, P01HL069020] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG028787, R01AG023039] Funding Source: NIH RePORTER
- NHLBI NIH HHS [HL69020, HL 59139, HL67724] Funding Source: Medline
- NIA NIH HHS [AG23039, AG28787] Funding Source: Medline
The prevalence of heart diseases, such as coronary artery disease and congestive heart failure, increases with age. Optimal therapeutic interventions that antagonize aging may reduce the occurrence and mortality of adult heart diseases. We discuss here how molecular mechanisms mediating life span extension affect aging of the heart and its resistance to pathological insults. In particular, we review our recent findings obtained from transgenic mice with cardiac-specific overexpression of Sirt1, which demonstrated delayed aging and protection against oxidative stress in the heart. We propose that activation of known longevity mechanisms in the heart may represent a novel cardioprotection strategy against aging and certain types of cardiac stress, such as oxidative stress.
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