Cited by 179Autophagy in Disease and TherapyGenetics, Aging, and Longevity in Model OrganismsDietary Effects on Health

Autophagy in the heart and liver during normal aging and calorie restriction

Wohlgemuth, Stephanie E., Julian, David, Akin, Debora E., Fried, Joanna, Toscano, Kristin, Leeuwenburgh, Christiaan, Dunn, Jr., William A.·2007·Rejuvenation Research

Abstract

Autophagy is a highly regulated intracellular process for the degradation of cellular constituents and essential for the maintenance of a healthy cell. We evaluated the effects of age and life-long calorie restriction on autophagy in heart and liver of young (6 months) and old (26 months) Fisher 344 rats. We observed that the occurrence of autophagic vacuoles was higher in heart than liver. The occurrence of autophagic vacuoles was not affected by age in either tissue, but was increased with calorie restriction in heart but not in liver. Next, we examined the expression of proteins involved in the formation and maturation of autophagosomes (beclin-1, LC3, Atg7, Atg9) or associated with autolysosomes and lysosomes (LAMP-1; cathepsin D). In hearts of both ad libitum -fed and calorie-restricted rats, we observed an increase in expression of beclin-1 and procathepsin D, but not mature cathepsin D, and a decrease in expression of LAMP-1 because of aging. In hearts, calorie restriction stimulated the expression of Atg7 and Atg9 and the lipidation of Atg8 (elevated LC3-II/I ratios) in aged rats. In hearts of ad libitum -fed rats, expression of Atg7 and lipidation of Atg8 were unaffected by age, while the cellular levels of Atg9 were lower in aged animals. Furthermore, we observed that the age- and diet-dependent expression levels of those proteins differed between heart and liver. In conclusion, autophagy in heart and liver did not decrease with age in ad libitum -fed rats, but was enhanced by calorie restriction in the heart. Thus, calorie restriction may mediate some of its beneficial effects by stimulating autophagy in the heart, indicating the potential for cardioprotective therapies.

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Crossref · 10.1089/rej.2006.0535

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Authors
Wohlgemuth, S. E., Julian, D., Akin, D. E., Fried, J., Toscano, K., Leeuwenburgh, C., & Dunn, Jr.
Affiliations
  • University of Florida (US)
  • Department of Anatomy and Cell Biology, College of Medicine, University of Florida, Gainesville, Florida.
Venue
Rejuvenation Research
Published
2007-09
Volume
10
Issue
3
Pages
281-292
ISSN
  • 1094-5458 (ISSN-L)
  • 1549-1684
  • 1557-8577
OpenAlex
W2076953907
Cited by
179
References
6
Citations by year
2026: 2 · 2025: 5 · 2024: 7 · 2023: 2 · 2022: 5 · 2021: 8 · 2020: 7 · 2019: 6 · 2018: 16 · 2017: 10 · 2016: 7 · 2015: 4 · 2014: 14 · 2013: 18 · 2012: 20
FWCI
8.06
Type
journal article
Language
en
Open access
closed
Locations
  • Rejuvenation Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (AG-21042, R01AG021042, P30AG028740)
  • National Cancer Institute (R01CA095552, CA-95552)
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Physiology › Dietary Effects on Health
Keywords
autophagy, caloric restriction, aging, heart, liver, autophagosomes, Beclin-1, LC3, ATG7, Atg9, ATG8 lipidation, LAMP1, cathepsin D, autophagosome maturation, cardioprotection
MeSH terms
Beclin-1, Aging, Animals, Autophagy, Cathepsin D, Heart, Lipids, Liver, Male, Myocardium, Rats, Inbred F344, Caloric Restriction, Myocytes, Cardiac, Microscopy, Electron, Transmission, Apoptosis Regulatory Proteins, Rats

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