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Age-related changes before and after imposition of hemodynamic stress in the mammalian heart
1First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
Insights
The aging mammalian heart shows reduced adaptation to hemodynamic stress but retains some resilience. Interventions targeting molecular and cellular pathways may offer antiaging benefits for the heart.
Area of Science:
- Cardiovascular Biology
- Gerontology
- Molecular Cardiology
Background:
- The mammalian heart ages concurrently with other organs, with complex inter-organ and intra-tissue interactions influencing age-related changes.
- Myocyte aging is modulated by autocrine and paracrine signaling from surrounding cells within the myocardial tissue.
Purpose of the Study:
- To review age-related changes in the mammalian heart, focusing on growth, aging, and responses to hemodynamic stress.
- To explore antiaging strategies at the molecular and cellular levels for the aging heart.
Main Methods:
- Review of existing literature on cardiac aging, molecular and cellular changes, and responses to hemodynamic challenges.
- Analysis of age-related alterations in gene expression (proto-oncogenes, heat shock proteins) under stress.
- Examination of interventions with potential antiaging effects on the heart.
Main Results:
- Aged hearts exhibit diminished induction of stress-response genes (proto-oncogenes, heat shock proteins) to milder hemodynamic stress (hypertension, ischemia).
- The senescent heart demonstrates attenuated adaptation to hemodynamic stress but can respond to severe stress comparably to younger hearts.
- Interventions targeting molecular and cellular mechanisms show promise for antiaging modulation of the heart.
Conclusions:
- The aging heart's adaptive capacity to hemodynamic stress is reduced, characterized by impaired stress-response gene activation.
- Despite limitations, the aged heart retains some ability to adapt to environmental changes.
- Targeted interventions offer potential for mitigating cardiac aging at the molecular and cellular levels.
Abstract:
This review focusses on the following issues: how the mammalian heart grows and ages; age-related changes in the mammalian heart before and after imposition of hemodynamic stress; and antiaging modulation in the mammalian heart. The heart and other organs grow and age together in the whole body, and interactions occur between these organs. Therefore, the age-related changes at the molecular and cellular level in the in vivo heart are the summation of the changes of the heart per se and the effects of other organs or tissues on the heart. Furthermore, myocytes grow and age under the influence of age-related changes in other myocytes and other types of cells in the myocardial tissue through autocrine or paracrine mechanisms, because myocytes are exposed to many biologically active substances which are released from those cells. Since hypertension and ischemia are very common hemodynamic events in aged hearts, the characteristics in aged hearts are discussed in terms of responses to hypertension or ischemia. The induction of proto-oncogenes and heat shock protein genes in response to milder hemodynamic stress such as pressure-overload and ischemia is diminished in aged hearts. However, the aged heart can respond to more severe stress to a level similar to that of young-adult hearts. Therefore, the senescent heart is characterized by its attenuated adaptation to hemodynamic stress and by its ability to adapt to limited environmental changes. Several interventions have antiaging effects on the heart at the molecular and cellular level.