Jose Malavet
Please click here to see the paper: https://www.frontiersin.org/articles/10.3389/fcvm.2021.757784/full
About the Authors: The Translational Cardiovascular Disease Research Laboratory of principal investigator DeLisa Fairweather, Ph.D., studies the identification of biomarkers that can be used as diagnostic and therapeutic targets for cardiovascular and autoimmune diseases. Our lab, which is located at Mayo Clinic in Jacksonville, Florida, focuses on several areas of research, including: Discovering individualized therapies and improved diagnoses for chronic inflammatory diseases Understanding how sex differences in inflammation caused by environmental exposures can lead to chronic inflammatory diseases. Examining the immunopathogenesis of myocarditis, dilated cardiomyopathy and heart failure, our goal is to develop research breakthroughs by better understanding the pathogenesis of disease characterized by sex differences. Dr. Fairweather and her research team ultimately hope to discover new diagnostic techniques and novel therapies for patients with myocarditis and other cardiovascular and autoimmune diseases.
About the Work: The study investigates the role of TRPC6, a gene associated with doxorubicin-induced cardiotoxicity, as a potential therapeutic target for mitigating chemotherapy-related heart damage. The research, conducted on male and female mice, involved administering doxorubicin, a commonly used chemotherapy drug, to assess cardiac damage and function. Male mice lacking the Trpc6 gene exhibited significant improvement in cardiac damage markers, including reduced vacuolation, fibrosis, and Myh7 expression, along with increased Tnni3 expression. Cardiac function, evaluated through echocardiography, also showed improvement in Trpc6-deficient male mice. Although female mice were less susceptible to doxorubicin-induced damage, Trpc6-deficient females displayed improved vacuolation. The study underscores the role of TRPC6 in promoting doxorubicin-induced cardiomyopathy in male mice, suggesting its potential as a therapeutic target. Sex differences were observed in response to doxorubicin, indicating a more robust ability of female mice to modulate other Trpc channels and Rcan1 expression. These findings contribute to understanding the molecular mechanisms underlying chemotherapy-related cardiotoxicity and highlight potential avenues for cardioprotective interventions.
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