Ciencias Exactas y Ciencias de la Salud
Permanent URI for this collectionhttps://hdl.handle.net/11285/551039
Pertenecen a esta colección Tesis y Trabajos de grado de las Maestrías correspondientes a las Escuelas de Ingeniería y Ciencias así como a Medicina y Ciencias de la Salud.
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- Characterization of the cytotoxicity of graphene oxide and reduced graphene oxide in hypertrophic cardiomyocytes(Instituto Tecnológico y de Estudios Superiores de Monterrey, 2020-06-15) Luna Figueroa, Estefanía; GARCIA RIVAS, GERARDO DE JESUS; 43362; García Rivas, Gerardo de Jesús; emipsanchez/puemcuervo; Castorena Torres, Fabiola; Aguirre Tostado, Francisco Servando; Lozano García, Omar; Escuela de Medicina y Ciencias de la Salud; Campus Monterrey; Contreras Torres, Flavio FernandoGraphene oxide (GO) and reduced graphene oxide (RGO) are carbon nanomaterials, which stand out for their industrial and biomedical use due to their extraordinary physicochemical properties. Nevertheless, possible health risks call into question the benefits derived from its use. In particular, our interest is focused on cardiovascular tissue. Accumulation of particles in the myocardium may be feasible in this type of tissue, a risk that is more severe in tissues with a predisposition to damage. Even at low concentrations of particles, the risk ratio indicates the possibility of cardiometabolic disorders. The present study analyzes the cytotoxicity of GO and RGO in healthy cardiomyoblasts and cardiomyoblasts with cellular damage, using a pathological model of angiotensin II-induced hypertrophy. From the results obtained, we proposed possible mechanisms of cellular damage.
- The role of the mitochondrial calcium uniporter in the process of arrhythmogenesis in a murine model of acute catecholamine overload(Instituto Tecnológico y de Estudios Superiores de Monterrey, 2020-05-22) Salazar Ramírez, Felipe de Jesús; SALAZAR RAMIREZ, FELIPE DE JESUS; 876167; García Rivas, Gerardo de Jesús; emipsanchez; Alves Figueiredo, Hugo Jorge; Rojas Martínez, Augusto; Ramos Mondragón, Roberto; Escuela de Medicina y Ciencias de la Salud; Campus MonterreySudden cardiac death by fulminant ventricular arrhythmias remains a concern in population with cardiac risk. Recently, the mitochondrion has been implied to be a central player in Ca2+ mishandling, with its dysfunction leading up to arrhythmogenesis. A possible starting event that could lead to most changes seen in cardiac disfunction is mitochondrial Ca2+ overload. The following research study focuses on demonstrating the effects of mitochondrial Ca2+ influx inhibition in arrhythmogenesis. A murine model of acute catecholamine (isoproterenol) overload was treated previously with mitochondrial Ca2+ transport inhibitor Ru360. Ru360 treated mice showed a complete abolishment of ventricular tachycardia and ventricular fibrillation. To characterize the possible mechanisms of action, heart mitochondria were isolated and mitochondrial function was assessed. Mitochondrial Ca2+ transport inhibition preserved mitochondrial function and membrane integrity as demonstrated by a higher respiratory control and calcium retention capacity when compared to isoproterenol-treated mice which appears to be caused by a reduced oxidative stress as a trend to preserve reduced thiol groups was shown. Given the positive results obtained in abolishing ventricular arrhythmias by inhibiting mitochondrial Ca2+ transport, it is precise to continue the characterization of the mechanisms by which this therapy exerts its effects. To fully demonstrate its efficacy and characterize its mechanism of action may lead up to a new therapeutic target and therapy that could set the bases to clinical research in the near future.