by Acín-Pérez, Rebeca, Lechuga-Vieco, Ana Victoria, Del Mar Muñoz, Maria, Nieto-Arellano, Rocio, Torroja, Carlos, Sanchez-Cabo, Fatima, Jiménez, Concepción, González-Guerra, Andrés, Carrascoso, Isabel, Benincá, Cristiane, Quiros, Pedro M, López-Otín, Carlos, Castellano, José María, Ruiz-Cabello, Jesus, Jimenez-Borreguero, Luis Jesús and Enríquez, José Antonio
Abstract:
Heart failure (HF) is a major health and economic burden in developed countries. It has been proposed that the pathogenesis of HF may involve the action of mitochondria. We evaluate three different mouse models of HF: tachycardiomyopathy, HF with preserved left ventricular (LV) ejection fraction (LVEF), and LV myocardial ischemia and hypertrophy. Regardless of whether LVEF is preserved, our results indicate that the three models share common features: an increase in mitochondrial reactive oxygen species followed by ultrastructural alterations in the mitochondrial cristae and loss of mitochondrial integrity that lead to cardiomyocyte death. We show that the ablation of the mitochondrial protease OMA1 averts cardiomyocyte death in all three murine HF models, and thus loss of OMA1 plays a direct role in cardiomyocyte protection. This finding identifies OMA1 as a potential target for preventing the progression of myocardial damage in HF associated with a variety of etiologies.
Reference:
Ablation of the stress protease OMA1 protects against heart failure in mice. (Acín-Pérez, Rebeca, Lechuga-Vieco, Ana Victoria, Del Mar Muñoz, Maria, Nieto-Arellano, Rocio, Torroja, Carlos, Sanchez-Cabo, Fatima, Jiménez, Concepción, González-Guerra, Andrés, Carrascoso, Isabel, Benincá, Cristiane, Quiros, Pedro M, López-Otín, Carlos, Castellano, José María, Ruiz-Cabello, Jesus, Jimenez-Borreguero, Luis Jesús and Enríquez, José Antonio), In Science Translational Medicine, volume 10, 2018.
Bibtex Entry:
@article{AcinPerez:2018jm,
author = {Ac{'i}n-P{'e}rez, Rebeca and Lechuga-Vieco, Ana Victoria and Del Mar Mu{~n}oz, Maria and Nieto-Arellano, Rocio and Torroja, Carlos and Sanchez-Cabo, Fatima and Jim{'e}nez, Concepci{'o}n and Gonz{'a}lez-Guerra, Andr{'e}s and Carrascoso, Isabel and Beninc{'a}, Cristiane and Quiros, Pedro M and L{'o}pez-Ot{'i}n, Carlos and Castellano, Jos{'e} Mar{'i}a and Ruiz-Cabello, Jesus and Jimenez-Borreguero, Luis Jes{'u}s and Enr{'i}quez, Jos{'e} Antonio},
title = {{Ablation of the stress protease OMA1 protects against heart failure in mice.}},
journal = {Science Translational Medicine},
year = {2018},
volume = {10},
number = {434},
pages = {eaan4935},
month = mar,
affiliation = {Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid 28029, Spain. jaenriquez@cnic.es rebeca.acin@cnic.es.},
doi = {10.1126/scitranslmed.aan4935},
pmid = {29593106},
language = {English},
rating = {0},
date-added = {2018-04-04T07:26:13GMT},
date-modified = {2019-10-09T09:21:58GMT},
abstract = {Heart failure (HF) is a major health and economic burden in developed countries. It has been proposed that the pathogenesis of HF may involve the action of mitochondria. We evaluate three different mouse models of HF: tachycardiomyopathy, HF with preserved left ventricular (LV) ejection fraction (LVEF), and LV myocardial ischemia and hypertrophy. Regardless of whether LVEF is preserved, our results indicate that the three models share common features: an increase in mitochondrial reactive oxygen species followed by ultrastructural alterations in the mitochondrial cristae and loss of mitochondrial integrity that lead to cardiomyocyte death. We show that the ablation of the mitochondrial protease OMA1 averts cardiomyocyte death in all three murine HF models, and thus loss of OMA1 plays a direct role in cardiomyocyte protection. This finding identifies OMA1 as a potential target for preventing the progression of myocardial damage in HF associated with a variety of etiologies.},
url = {http://stm.sciencemag.org/lookup/doi/10.1126/scitranslmed.aan4935},
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uri = {url{papers3://publication/doi/10.1126/scitranslmed.aan4935}}
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