Detalles del proyecto
Descripción
Perilipin family proteins (PLIN) regulate lipid storage metabolism through of coating of intracellular neutral lipids in structures called lipid droplets (LD). PLIN proteins differ in size, affinity for LD, tissue expression, transcriptional regulation, and unbound stability. PLIN5 is expressed mainly in cardiac muscle, and its main function is to protect the heart from oxidative damage by sequestering fatty acid (FA) and by forming lipid barriers of uncontrolled mobilization of triacylglycerols, and excessive release and oxidation of FA. However, the participation of PLIN family in physiologic hypertrophy induced by pregnancy and its reversible process (postpartum) are not well defined. Because pregnancy induces physiologic hypertrophy and is a natural reversible process, the in-depth analyses of the biochemical and physiological mechanisms of substrate metabolism that occur before, during and after pregnancy provide an ideal opportunity to study a natural biological process that does not require genetic modification or exogenous manipulation of the behavior to explore the mechanisms of the pathological hypertrophy associated with the reprogramming of cardiac metabolism. Furthermore, the study of rats, which have short-term and easy to track pregnancies, make them logistically accessible for conducting the proposed research. Therefore, the goal of this proposal is to evaluate the contributions of the Perilipin family axis activation before, during, and after pregnancy to lipid metabolism in the left ventricle, which is most susceptible to hypertrophy. The specific aims will address the central hypothesis that PLIN family are activated to coordinate the cardiac lipid metabolism during pregnancy and that their activation is reversible during postpartum to the maintain cardiac function and structure.
Tipo de cooperación con otras instituciones
Internacional
Tipo de financiamiento
Collaborative Grant UC Mexus CONACYT
Tipo de investigación
Basica
Estado | Finalizado |
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Fecha de inicio/Fecha fin | 1/07/19 → 31/07/21 |
Huella digital
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