Key result
Testosterone reduces cardiac remodeling and cuts MMP-3 expression ~33% after myocardial ischemia/reperfusion injury.
Why the study?
The role of testosterone metabolism via aromatase and 5α-reductase enzymes in myocardial remodeling after ischemia/reperfusion injury in gonadectomized rats is poorly understood.
Answers are grounded in this paper and cite their sources.
May attenuate post-I/R remodeling in hypogonadal rat models; hypothesis-generating and leaves open human translation.
The effects of testosterone on cardiovascular homeostasis are still not well understood. The objective of this work was to evaluate the effects of testosterone in the absence or presence of inhibition of Aromatase (4-hydroxyandrostenedione) and/or 5α reductase (Finasteride) enzymatic activities on the myocardial remodeling 30 days after ischemia/reperfusion (I/R) injury in gonadectomized rats. Results showed that testosterone administration to ORX rats resulted in decreased myocardial damaged area, inflammatory infiltrates and reduced MMP-3 and 13 expressions. Interestingly, Finasteride administration resulted in a greater decrease in scar tissue, inflammatory infiltrates, along with a significant decrease in MMP-3 and 13 expressions. In contrast, 4-hydroxyandrostenedione administrations increased all parameters. Our results suggest that testosterone does not have a direct effect since simultaneous inhibition of aromatase and 5α-reductase did not induce significant changes in I/R induced myocardial injury.
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Maldonado et al. (2019) studied Ischemia/reperfusion-induced myocardial damage (n=55). Testosterone vs. Vehicle control was evaluated on MMP-3 expression (integrated optical density) (p=<0.05). Testosterone administration significantly decreased cardiac remodeling and MMP-3 expression in orchidectomized rats after 30 days of ischemia/reperfusion-induced myocardial damage.
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