Sex Determines Cardiac Myocyte Stretch and Relaxation
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Biological Sex Determines Cardiomyocyte Stretch and Relaxation
Trexler et al1 show for the first time that biological sex differences in isolated rat cardiomyocytes and myofibrils affect myocyte function. In addition, they discovered sex-specific cardiomyocyte gene expression profiles, like the protein kinase A pathway, that could provide insight into sex differences in cardiovascular diseases (CVDs). This study reports sex differences in gene profiles of isolated cardiomyocytes using high-quality RNAseq data, which allows a more detailed look at gene differences than previously published gene expression studies that typically used microarray of whole hearts (a combination of myocytes, fibroblasts, endothelial, and resident immune cells, for example).2,3 A major finding of Trexler et al1 is that healthy female rats have increased fractional shortening in both whole hearts and in paced cardiomyocytes. Female cardiac myocytes and myofibrils also take longer to relax after contraction, which may contribute to cardiac dysfunction in women after cardiac injury or disease.
See Article by Trexler et al
Sex Differences in Cardiac Physiology That Influence CVD
CVD is the leading cause of death in men and women worldwide.4 Before age 60, men are at an increased risk of death because of heart failure, whereas women develop some forms of heart disease, like stroke and hypertension, more frequently after menopause.4,5 Historically, women have been underrepresented in cardiovascular clinical trials.6 This led to the National Institutes of Health requirement to include women in clinical trials with the unexpected outcome that the data were in most cases not being analyzed according to sex. Controlling for sex or examining only one sex is not sufficient to understand the reason for sex (biological) and gender (social) differences in CVD and other chronic diseases.7 …