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Heart Failure as an Aging-Related Phenotype.
Hiroyuki Morita1, Issei Komuro1
1Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo.
International Heart Journal
|January 16, 2018
Summary
Heart failure involves aging processes. This review explores how Wnt/β-catenin signaling and the p53 pathway contribute to heart failure pathophysiology, highlighting C1q
Area of Science:
- Cardiovascular Biology
- Molecular Gerontology
- Pathophysiology
Background:
- Heart failure is a major cause of mortality with incompletely understood molecular mechanisms.
- It is recognized as a systemic syndrome linked to aging-related phenotypes.
- Key aging regulators, Wnt/β-catenin signaling and the p53 pathway, are implicated in heart failure pathogenesis.
Purpose of the Study:
- To review recent advancements in understanding the molecular pathophysiology of heart failure.
- To focus on the roles of Wnt/β-catenin signaling and the p53 pathway in heart failure.
- To highlight the interplay between cardiomyocytes and non-cardiomyocytes in heart failure.
Main Methods:
- Literature review of molecular mechanisms in heart failure.
- Analysis of the involvement of Wnt/β-catenin signaling.
- Examination of the role of the p53 pathway in cardiomyocyte apoptosis.
Main Results:
- Circulating C1q activates Wnt/β-catenin signaling, promoting aging phenotypes like sarcopenia and heart failure.
- The p53 pathway induces apoptosis in cardiomyocytes within the failing heart.
- Cross-talk between cardiomyocytes and non-cardiomyocytes is a significant aspect of heart failure molecular mechanisms.
Conclusions:
- Wnt/β-catenin signaling and the p53 pathway are critical molecular players in heart failure.
- C1q acts as a novel activator of Wnt/β-catenin signaling, linking aging to heart failure.
- Understanding these pathways and cell-cell interactions is crucial for future heart failure research.
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