Naroa Goikoetxea-Usandizaga, Marina Serrano-Maciá, Teresa C Delgado, Jorge Simón, David Fernández Ramos, Diego Barriales, Maria E Cornide, Mónica Jiménez, Marina Pérez-Redondo, Sofia Lachiondo-Ortega, Rubén Rodríguez-Agudo, Maider Bizkarguenaga, Juan Diego Zalamea, Samuel T Pasco, Daniel Caballero-Díaz, Benedetta Alfano, Miren Bravo, Irene González-Recio, Maria Mercado-Gómez, Clàudia Gil-Pitarch, Jon Mabe, Jordi Gracia-Sancho, Leticia Abecia, Óscar Lorenzo, Paloma Martín-Sanz, Nicola G A Abrescia, Guadalupe Sabio, Mercedes Rincón, Juan Anguita, Eduardo Miñambres, César Martín, Marina Berenguer, Isabel Fabregat, Marta Casado, Carmen Peralta, Marta Varela-Rey, María Luz Martínez-Chantar
BACKGROUND AND AIMS: Hepatic ischemia-reperfusion injury (IRI) is the leading cause of early posttransplantation organ failure as mitochondrial respiration and ATP production are affected. A shortage of donors has extended liver donor criteria, including aged or steatotic livers, which are more susceptible to IRI. Given the lack of an effective treatment and the extensive transplantation waitlist, we aimed at characterizing the effects of an accelerated mitochondrial activity by silencing methylation-controlled J protein (MCJ) in three preclinical models of IRI and liver regeneration, focusing on metabolically compromised animal models...
March 2022: Hepatology: Official Journal of the American Association for the Study of Liver Diseases