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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 2586706, 13 pages
Research Article

HSP27 Alleviates Cardiac Aging in Mice via a Mechanism Involving Antioxidation and Mitophagy Activation

1Department of Geriatrics, First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China
2Department of Anesthesiology, First Affiliated Hospital with Nanjing Medical University, Nanjing 210029, China
3Department of Surgery, East Tennessee State University, Johnson City, TN 37614, USA
4Department of Pathophysiology, Nanjing Medical University, Nanjing 210029, China

Received 30 September 2015; Revised 30 January 2016; Accepted 22 February 2016

Academic Editor: Alessandra Ricelli

Copyright © 2016 Shenglan Lin et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 old WT 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 old WT 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 old WT hearts. Additionally, old Tg hearts had higher levels of PINK1 and Parkin than old WT hearts, suggesting that mitophagy was activated in old Tg hearts. Taken together, HSP27 alleviated cardiac aging and this action involved antioxidation and mitophagy activation.