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AGE

, Volume 35, Issue 6, pp 2177–2182 | Cite as

Calorie restriction can reverse, as well as prevent, aging cardiomyopathy

  • Lin YanEmail author
  • Shumin Gao
  • David Ho
  • Misun Park
  • Hui Ge
  • Chunbo Wang
  • Yimin Tian
  • Lo Lai
  • Mariana S. De Lorenzo
  • Dorothy E. Vatner
  • Stephen F. Vatner
Article

Abstract

Calorie restriction (CR) is the most widely studied intervention protecting from the adverse effects of aging. Almost all prior studies have examined the effects of CR initiated in young animals. Studies examining the effects of CR on development of aging cardiomyopathy found only partial prevention. The major goal of this study was to determine whether CR initiated after aging cardiomyopathy developed could reverse the cardiomyopathy. Aging cardiomyopathy in 2-year-old mice was characterized by reduced left ventricular (LV) function, cardiac hypertrophy, and increased cardiac apoptosis and fibrosis. When short-term (2 months) CR was initiated after aging cardiomyopathy developed in 20-month-old mice, the decrease in cardiac function, and increases in LV weight, myocardial fibrosis and apoptosis were reversed, such that the aging hearts in these mice were indistinguishable from those of young mice or mice where CR was initiated in young mice. If apoptosis was the mechanism for protecting against aging cardiomyopathy, then total myocyte numbers should have reverted to normal with CR, but did not. However, the alterations in cytoskeletal proteins, which contribute to aging cardiomyopathy, were no longer observed with CR. This is the first study to demonstrate complete prevention of aging cardiomyopathy by CR and, more importantly, that instituting this intervention even later in life can rapidly correct aging cardiomyopathy, which could have important therapeutic implications.

Keywords

Calorie restriction Aging Cardiomyopathy Apoptosis Myocyte loss 

Notes

Acknowledgments

We thank Serge Salganik for statistical analysis and Dr. Doru Chirieac for technical help. This work was supported by the National Institute of Health grants 5P01AG027211, 5R21HL097264, 1R01HL102472, 5R01HL033107, 5T32HL069752, 5R01HL095888, 5P01HL069020, and 5R01HL091781.

Supplementary material

11357_2012_9508_MOESM1_ESM.docx (39 kb)
ESM 1 (DOCX 38 kb)

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Copyright information

© American Aging Association 2013

Authors and Affiliations

  • Lin Yan
    • 1
    Email author
  • Shumin Gao
    • 1
  • David Ho
    • 1
  • Misun Park
    • 1
  • Hui Ge
    • 1
  • Chunbo Wang
    • 1
  • Yimin Tian
    • 1
  • Lo Lai
    • 1
  • Mariana S. De Lorenzo
    • 1
  • Dorothy E. Vatner
    • 1
  • Stephen F. Vatner
    • 1
  1. 1.Department of Cell Biology and Molecular Medicine, Cardiovascular Research InstituteUMDNJ-New Jersey Medical SchoolNewarkUSA

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