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Heartfulness: Contributors of Healthy and Unhealthy Cardiac Aging

Special Issue Editors


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Guest Editor
1. Laboratory of Metabolism and Exercise (LaMetEx) Research Center in Physical Activity, Health and Leisure (CIAFEL) and Laboratory for Integrative and Translational Research in Population Health (ITR), Faculty of Sports, University of Porto (FADEUP), 4200-450 Porto, Portugal
2. CNC - Center for Neuroscience and Cell Biology, CIBB - Centre for Innovative Biomedicine and Biotechnology, University of Coimbra, 3004-504 Coimbra, Portugal
3. IIIUC - Institute for Interdisciplinary Research, University of Coimbra, 3030-789 Coimbra, Portugal
Interests: developmental origins of health and disease; metabolic programming; bioenergetics; cardiac mitochondria; energy metabolism; cardiovascular aging and diseases
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Guest Editor
1. Center for Precision Medicine, Wake Forest University Health Sciences, Winston-Salem, NC 27157, USA
2. Section on Molecular Medicine, Department of Internal Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA
Interests: developmental origins of health and disease; cardiometabolic programming; integrated omic approaches to investigate cardiovascular aging and diseases

Special Issue Information

Dear Colleagues,

Healthy cardiac aging involves maintaining optimal heart function throughout one’s lifespan, while unhealthy cardiac aging refers to the decline in heart health and the increased risk of cardiovascular disease as a person ages. Both healthy and unhealthy cardiac aging are influenced by a wide range of factors, including genetics, environmental factors, and lifestyle habits, such as regular exercise, healthy diet, stress management, adequate sleep, and avoiding smoking and excessive alcohol consumption, among others.

Although extensive research has been conducted on cardiac aging, there are still many unknowns about this process. Some areas that require further investigation include:

  • Mechanisms of cardiac aging: While aging is known to cause changes in the heart, the exact mechanisms and the molecular and cellular processes behind these changes are still not fully understood.
  • Factors that influence cardiac aging: While there are known risk factors for cardiovascular disease, such as smoking and high blood pressure, it is not fully understood how these factors contribute to cardiac aging. Additionally, there may be other genetic, environmental, and lifestyle factors that influence the aging process in the heart, which are not yet fully understood.
  • Gender differences: There are known differences between men and women when it comes to the risk of cardiovascular disease and the aging process of the heart. However, the mechanisms behind these differences are still not fully understood.
  • Long-term effects: The long-term effects of cardiac aging on overall health and quality of life are not fully understood. Additionally, there may be differences in the long-term effects of cardiac aging between different populations and individuals.
  • Potential interventions: While healthy lifestyle habits can promote healthy cardiac aging, there are currently no known interventions or treatments that can halt or reverse the aging process in the heart. Researchers are still exploring potential therapies and interventions that could help prevent or slow the progression of cardiac aging.

A better understanding of the regulatory networks in cardiac development and aging are a prerequisite for the development of therapies to treat a range of heart diseases from congenital abnormalities to adult cardiomyopathies.

We count on your cutting-edge research and contribution to uncover critical components of both cardiac developmental pathways and aging mechanisms to inspire novel therapeutic strategies to treat human heart failure. We welcome original research and review manuscripts on any aspects of healthy and unhealthy cardiac aging.

Dr. Susana P. Pereira
Prof. Dr. Laura A. Cox
Guest Editors

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Keywords

  • cardiac development
  • gene regulation
  • epigenetics
  • genomics
  • integrated omics
  • accelerated aging
  • cardiac metabolism
  • cardiac regeneration and repair
  • cardiovascular diseases
  • cutting-edge techniques
  • cardiac imaging
  • regenerative mechanisms
  • pathophysiology of cardiovascular disease
  • cardiac endothelium
  • cardiomyocytes
  • cardiovascular computational modeling
  • cardiovascular informatics
  • transgenerational inheritance
  • life expectancy

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Published Papers (1 paper)

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28 pages, 2913 KiB  
Article
Characterizing Early Cardiac Metabolic Programming via 30% Maternal Nutrient Reduction during Fetal Development in a Non-Human Primate Model
by Susana P. Pereira, Mariana S. Diniz, Ludgero C. Tavares, Teresa Cunha-Oliveira, Cun Li, Laura A. Cox, Mark J. Nijland, Peter W. Nathanielsz and Paulo J. Oliveira
Int. J. Mol. Sci. 2023, 24(20), 15192; https://doi.org/10.3390/ijms242015192 - 14 Oct 2023
Cited by 3 | Viewed by 2440
Abstract
Intra-uterine growth restriction (IUGR) is a common cause of fetal/neonatal morbidity and mortality and is associated with increased offspring predisposition for cardiovascular disease (CVD) development. Mitochondria are essential organelles in maintaining cardiac function, and thus, fetal cardiac mitochondria could be responsive to the [...] Read more.
Intra-uterine growth restriction (IUGR) is a common cause of fetal/neonatal morbidity and mortality and is associated with increased offspring predisposition for cardiovascular disease (CVD) development. Mitochondria are essential organelles in maintaining cardiac function, and thus, fetal cardiac mitochondria could be responsive to the IUGR environment. In this study, we investigated whether in utero fetal cardiac mitochondrial programming can be detectable in an early stage of IUGR pregnancy. Using a well-established nonhuman IUGR primate model, we induced IUGR by reducing by 30% the maternal diet (MNR), both in males (MNR-M) and in female (MNR-F) fetuses. Fetal cardiac left ventricle (LV) tissue and blood were collected at 90 days of gestation (0.5 gestation, 0.5 G). Blood biochemical parameters were determined and heart LV mitochondrial biology assessed. MNR fetus biochemical blood parameters confirm an early fetal response to MNR. In addition, we show that in utero cardiac mitochondrial MNR adaptations are already detectable at this early stage, in a sex-divergent way. MNR induced alterations in the cardiac gene expression of oxidative phosphorylation (OXPHOS) subunits (mostly for complex-I, III, and ATP synthase), along with increased protein content for complex-I, -III, and -IV subunits only for MNR-M in comparison with male controls, highlight the fetal cardiac sex-divergent response to MNR. At this fetal stage, no major alterations were detected in mitochondrial DNA copy number nor markers for oxidative stress. This study shows that in 90-day nonhuman primate fetuses, a 30% decrease in maternal nutrition generated early in utero adaptations in fetal blood biochemical parameters and sex-specific alterations in cardiac left ventricle gene and protein expression profiles, affecting predominantly OXPHOS subunits. Since the OXPHOS system is determinant for energy production in mitochondria, our findings suggest that these early IUGR-induced mitochondrial adaptations play a role in offspring’s mitochondrial dysfunction and can increase predisposition to CVD in a sex-specific way. Full article
(This article belongs to the Special Issue Heartfulness: Contributors of Healthy and Unhealthy Cardiac Aging)
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