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.

Browse

Filters

20201

Settings

¡Quiero depositar mi trabajo!
Author: search.filters.author.Salazar Ramírez, Felipe de JesúsSubject: search.filters.subject.Arrhythmia

Search Results

Now showing 1 - 1 of 1
  • Thumbnail Image
    Tesis de maestría
    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 Monterrey
    Sudden 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.
En caso de no especificar algo distinto, estos materiales son compartidos bajo los siguientes términos: Atribución-No comercial-No derivadas CC BY-NC-ND http://www.creativecommons.mx/#licencias
logo

El usuario tiene la obligación de utilizar los servicios y contenidos proporcionados por la Universidad, en particular, los impresos y recursos electrónicos, de conformidad con la legislación vigente y los principios de buena fe y en general usos aceptados, sin contravenir con su realización el orden público, especialmente, en el caso en que, para el adecuado desempeño de su actividad, necesita reproducir, distribuir, comunicar y/o poner a disposición, fragmentos de obras impresas o susceptibles de estar en formato analógico o digital, ya sea en soporte papel o electrónico. Ley 23/2006, de 7 de julio, por la que se modifica el texto revisado de la Ley de Propiedad Intelectual, aprobado

DSpace software copyright © 2002-2025

Licencia