Cannabidiol Prevents Heart Failure Dysfunction and Remodeling Through Preservation of Mitochondrial Function and Calcium Handling.

大麻二酚通过保护线粒体功能和钙处理来预防心力衰竭功能障碍和重塑

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作者:García-Rivas Gerardo, Lozano Omar, Bernal-Ramírez Judith, Silva-Platas Christian, Salazar-Ramírez Felipe, Méndez-Fernández Abraham, Morales-Ochoa Carolina, Alves-Figueiredo Hugo, Ramos-González Martín Rogelio, Rubio-Infante Nestor, Vázquez-Garza Eduardo, Luévano-Martínez Luis A, López-Morán Silvia, Chapoy-Villanueva Héctor, Bolton James, Velasco-Bolom José-Luis, Mendoza-Espinosa Paola, Contreras-Torres Flavio F, Jerjes-Sánchez Carlos, Torre-Amione Guillermo
Heart failure (HF) is characterized by energy deprivation, calcium (Ca(2+)) handling alterations, and inflammation: effects associated with mitochondrial dysfunction. Cannabidiol previously prevented mitochondrial dysfunction. Thus, it may prevent HF progression. In mice with HF, subcutaneous cannabidiol attenuated cardiac fibrosis, hypertrophy, loss of ejection fraction, and inflammation; isolated cardiomyocytes preserved cell shortening, Ca(2+) handling, mitochondrial function and redox balance. Hypertrophied ventricular cardiomyoblasts suggested cannabidiol-mediated effects through peroxisome proliferator-activated gamma receptors. Therefore, cannabidiol in HF limited cardiac hypertrophy and preserved contractile function by sustaining cardiomyocyte and mitochondrial function through redox balance maintenance, supporting cannabidiol role as a cardioprotective therapy in HF.

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