期刊
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
卷 2016, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2016/2586706
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类别
资金
- National Natural Science Foundation of China [81571290, 81571378, 81370260, 81371450, 81170321]
- Jiangsu Province's Outstanding Medical Academic Leader Program [LJ201124]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD)
- Collaborative Innovation Center for Cardiovascular Disease Translational Medicine
Aging-induced cardiac dysfunction is a prominent feature of cardiac aging. Heat shock protein 27 (HSP27) protects cardiac function against ischemia or chemical challenge. We hypothesized that HSP27 attenuates cardiac aging. Transgenic (Tg) mice with cardiac-specific expression of the HSP27 gene and wild-type (WT) littermates were employed in the experiments. Echocardiography revealed a significant decline in the cardiac function of old WT mice compared with young WT mice. In striking contrast, the aging-induced impairment of cardiac function was attenuated in old Tg mice compared with oldWT mice. Levels of cardiac aging markers were lower in old Tg mouse hearts than in old WT mouse hearts. Less interstitial fibrosis and lower contents of reactive oxygen species and ubiquitin-conjugated proteins were detected in old Tg hearts than in oldWT hearts. Furthermore, old Tg hearts demonstrated lower accumulation of LC3-II and p62 than old WT hearts. Levels of Atg13, Vps34, and Rab7 were also higher in old Tg hearts than in oldWT hearts. Additionally, old Tg hearts had higher levels of PINK1 and Parkin than oldWT hearts, suggesting that mitophagy was activated in old Tg hearts. Taken together, HSP27 alleviated cardiac aging and this action involved antioxidation and mitophagy activation.
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