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Early Development of Cardiac Fibrosis in Young Old-Father Offspring
A Ismail1, Y Saliba1, N Fares1
1Physiology and Pathophysiology Research Laboratory, Pole of Technology and Health, Faculty of Medicine, Saint Joseph University, Beirut, Lebanon.
Oxidative Medicine and Cellular Longevity
|October 4, 2022
Summary
Advanced paternal age in rats leads to cardiac fibrosis and hypertrophy in offspring, even under stress. This suggests intergenerational transmission of cardiac remodeling risk factors from fathers to young progeny.
Area of Science:
- Cardiovascular Biology
- Aging Research
- Reproductive Biology
Background:
- Cardiac aging is linked to progressive fibrosis.
- Advanced paternal age is epidemiologically associated with increased heart failure risk in offspring.
Purpose of the Study:
- To investigate the impact of paternal age on cardiac phenotype in young male rat offspring under circulatory stress.
- To explore the mechanisms behind paternal age-related cardiac remodeling.
Main Methods:
- Mating old males with young females vs. young males with young females to produce offspring.
- Inducing hypertension using N(ω)-nitro-L-arginine methyl ester (L-NAME) in offspring.
- Analyzing cardiac hypertrophy, fibrosis, gene expression (Tcf21, Tbx18, Wt1), and protein pathways (TGF-β2).
Main Results:
- Offspring from old fathers (OFO) exhibited exacerbated cardiac hypertrophy and fibrosis compared to young father offspring (YFO) under L-NAME-induced hypertension.
- OFO hearts showed extracellular matrix expansion with epicardial fibroblast markers.
- The TGF-β2 receptor pathway was activated in OFO cardiac tissue, and increased cardiac DNA methylation was observed in old father offspring.
Conclusions:
- Advanced paternal age may be a risk factor for early cardiac fibrosis progression in young hypertensive offspring.
- Intergenerational transmission of cardiac remodeling may occur due to paternal age.
