Chapter 17 - Cardiac Aging

Dao-Fu Dai; Ying-Ann Chiao; Robert J Wessells; Rolf Bodmer; Hazel H Szeto; Peter S Rabinovitch

doi:10.1016/B978-0-12-411596-5.00017-4

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Book chapter

Chapter 17 - Cardiac Aging

Dao-Fu Dai, Ying-Ann Chiao, Robert J Wessells, Rolf Bodmer, Hazel H Szeto and Peter S Rabinovitch

Handbook of the Biology of Aging, pp.459-494

Elsevier Inc, Eighth Edition

2016

DOI: 10.1016/B978-0-12-411596-5.00017-4

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Abstract

Cardiovascular diseases are the leading causes of death in the western hemisphere. The exponential increases in the incidence and mortality rate of cardiovascular diseases in the elderly suggest that age per se is a major risk factor for cardiovascular diseases. The Framingham Heart Study and the Baltimore Longitudinal Study on Aging demonstrated that in the elderly human population there is an age-dependent increase in left ventricular hypertrophy, diastolic dysfunction, and a decrease in exercise capacity. Many of these changes are closely recapitulated in animal models commonly used in aging study, including rodents, flies, and monkeys. The conservation of intrinsic cardiac aging in the Drosophila melanogaster model offers unique genetic insights into cardiac aging. The application of genetically modified aged rodents elucidates several critical molecular mechanisms involved in cardiac aging, including mitochondrial oxidative stress, nutrient signaling, neurohormonal regulation-insulin/IGF/PI3K pathway, and the adrenergic and renin–angiotensin–aldosterone systems. In addition, aging of cardiac stem cells and decreased cardiac functional reserve in aging contribute to the susceptibility of aged hearts to stress and disease. We further discuss the mechanism of progression to heart failure in aged hearts. As the projected number of elderly persons is predicted to double in the next 25 years and the prevalence and economic burden of age-related cardiovascular disabilities continues to increase, there is an urgent need to understand the biology of the aging heart, the mechanisms for age-dependent cardiac vulnerability and to use these insights to develop strategies to prevent heart failure in the elderly. Finally, the potential clinical application of several “anti-aging” strategies to treat cardiovascular diseases and to improve healthy cardiac aging is summarized, including calorie restriction and its mimetics, strategies of mitochondrial intervention, and other novel agents.

heart failure

stem cells

calorie restriction

hypertrophy

mitochondria

diastolic function

arrhythmia

ros

Aging

angiotensin

adrenergic

mTOR

insulin-like growth factor

cardiac

rapamycin

Details

Title: Subtitle: Chapter 17 - Cardiac Aging
Creators: Dao-Fu Dai - Department of Pathology, University of Washington, Seattle, WA, USA
Ying-Ann Chiao - Department of Pathology, University of Washington, Seattle, WA, USA
Robert J Wessells - Geriatrics Center and Institute of Gerontology, University of Michigan, Ann Arbor, MI, USA
Rolf Bodmer - Development, Aging, and Regeneration Program Sanford-Burnham Medical Research Institute, La Jolla, CA, USA
Hazel H Szeto - Department of Pharmacology, Joan and Sanford I Weill Medical College of Cornell University, New York, NY, USA
Peter S Rabinovitch - Department of Pathology, University of Washington, Seattle, WA, USA
Resource Type: Book chapter
Publication Details: Handbook of the Biology of Aging, pp.459-494
Edition: Eighth Edition
DOI: 10.1016/B978-0-12-411596-5.00017-4
Publisher: Elsevier Inc
Language: English
Date published: 2016
Academic Unit: Pathology; Iowa Neuroscience Institute; Radiation Oncology
Record Identifier: 9984070627402771

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