eprintid: 124 rev_number: 10 eprint_status: archive userid: 2 importid: 0 dir: disk0/00/00/01/24 datestamp: 2021-06-01 23:55:10 lastmod: 2023-06-15 23:30:14 status_changed: 2021-06-01 23:55:10 type: article succeeds: 0 commentary: 0 metadata_visibility: show item_issues_count: 0 sword_depositor: 0 creators_name: Nicolás-Ávila, José A. creators_name: Lechuga-Vieco, Ana V. creators_name: Esteban-Martínez, Lorena creators_name: Sánchez-Díaz, María creators_name: Díaz-García, Elena creators_name: Santiago, Demetrio J. creators_name: Rubio-Ponce, Andrea creators_name: Li, Jackson LiangYao creators_name: Balachander, Akhila creators_name: Quintana, Juan A. creators_name: Martínez-de-Mena, Raquel creators_name: Castejón-Vega, Beatriz creators_name: Pun-García, Andrés creators_name: Través, Paqui G. creators_name: Bonzón-Kulichenko, Elena creators_name: García-Marqués, Fernando creators_name: Cussó, Lorena creators_name: A-González, Noelia creators_name: González-Guerra, Andrés creators_name: Roche-Molina, Marta creators_name: Martin-Salamanca, Sandra creators_name: Crainiciuc, Georgiana creators_name: Guzmán, Gabriela creators_name: Larrazabal, Jagoba creators_name: Herrero-Galán, Elías creators_name: Alegre-Cebollada, Jorge creators_name: Lemke, Greg creators_name: Rothlin, Carla V. creators_name: Jimenez-Borreguero, Luis Jesús creators_name: Reyes, Guillermo creators_name: Castrillo, Antonio creators_name: Desco, Manuel creators_name: Muñoz-Cánoves, Pura creators_name: Ibáñez, Borja creators_name: Torres, Miguel creators_name: Ng, Lai Guan creators_name: Priori, Silvia G. creators_name: Bueno, Héctor creators_name: Vázquez, Jesús creators_name: Cordero, Mario D. creators_name: Bernal, Juan A. creators_name: Enríquez, José A. creators_name: Hidalgo, Andrés creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: creators_id: mario.cordero@uneatlantico.es creators_id: creators_id: creators_id: title: A Network of Macrophages Supports Mitochondrial Homeostasis in the Heart ispublished: pub subjects: uneat_bm divisions: uneatlantico_produccion_cientifica full_text_status: none keywords: Macrophage; Mitochondria; Autophagy; Proteostasis; Phagocytosis; Heart. abstract: Cardiomyocytes are subjected to the intense mechanical stress and metabolic demands of the beating heart. It is unclear whether these cells, which are long-lived and rarely renew, manage to preserve homeostasis on their own. While analyzing macrophages lodged within the healthy myocardium, we discovered that they actively took up material, including mitochondria, derived from cardiomyocytes. Cardiomyocytes ejected dysfunctional mitochondria and other cargo in dedicated membranous particles reminiscent of neural exophers, through a process driven by the cardiomyocyte’s autophagy machinery that was enhanced during cardiac stress. Depletion of cardiac macrophages or deficiency in the phagocytic receptor Mertk resulted in defective elimination of mitochondria from the myocardial tissue, activation of the inflammasome, impaired autophagy, accumulation of anomalous mitochondria in cardiomyocytes, metabolic alterations, and ventricular dysfunction. Thus, we identify an immune-parenchymal pair in the murine heart that enables transfer of unfit material to preserve metabolic stability and organ function. date: 2020-10 date_type: published publication: Cell volume: 183 number: 1 pagerange: 94-109.e23 pages: 0 id_number: doi:10.1016/j.cell.2020.08.031 refereed: TRUE issn: 0092-8674 official_url: http://doi.org/10.1016/j.cell.2020.08.031 num_pieces: 0 gscholar_impact: 0 gscholar_datestamp: 0000-00-00 00:00:00 access: open language: en citation: Artículo Materias > Biomedicina Universidad Europea del Atlántico > Investigación > Producción Científica Abierto Inglés Cardiomyocytes are subjected to the intense mechanical stress and metabolic demands of the beating heart. It is unclear whether these cells, which are long-lived and rarely renew, manage to preserve homeostasis on their own. While analyzing macrophages lodged within the healthy myocardium, we discovered that they actively took up material, including mitochondria, derived from cardiomyocytes. Cardiomyocytes ejected dysfunctional mitochondria and other cargo in dedicated membranous particles reminiscent of neural exophers, through a process driven by the cardiomyocyte’s autophagy machinery that was enhanced during cardiac stress. Depletion of cardiac macrophages or deficiency in the phagocytic receptor Mertk resulted in defective elimination of mitochondria from the myocardial tissue, activation of the inflammasome, impaired autophagy, accumulation of anomalous mitochondria in cardiomyocytes, metabolic alterations, and ventricular dysfunction. Thus, we identify an immune-parenchymal pair in the murine heart that enables transfer of unfit material to preserve metabolic stability and organ function. metadata Nicolás-Ávila, José A.; Lechuga-Vieco, Ana V.; Esteban-Martínez, Lorena; Sánchez-Díaz, María; Díaz-García, Elena; Santiago, Demetrio J.; Rubio-Ponce, Andrea; Li, Jackson LiangYao; Balachander, Akhila; Quintana, Juan A.; Martínez-de-Mena, Raquel; Castejón-Vega, Beatriz; Pun-García, Andrés; Través, Paqui G.; Bonzón-Kulichenko, Elena; García-Marqués, Fernando; Cussó, Lorena; A-González, Noelia; González-Guerra, Andrés; Roche-Molina, Marta; Martin-Salamanca, Sandra; Crainiciuc, Georgiana; Guzmán, Gabriela; Larrazabal, Jagoba; Herrero-Galán, Elías; Alegre-Cebollada, Jorge; Lemke, Greg; Rothlin, Carla V.; Jimenez-Borreguero, Luis Jesús; Reyes, Guillermo; Castrillo, Antonio; Desco, Manuel; Muñoz-Cánoves, Pura; Ibáñez, Borja; Torres, Miguel; Ng, Lai Guan; Priori, Silvia G.; Bueno, Héctor; Vázquez, Jesús; Cordero, Mario D.; Bernal, Juan A.; Enríquez, José A. y Hidalgo, Andrés mail SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR, mario.cordero@uneatlantico.es, SIN ESPECIFICAR, SIN ESPECIFICAR, SIN ESPECIFICAR (2020) A Network of Macrophages Supports Mitochondrial Homeostasis in the Heart. Cell, 183 (1). 94-109.e23. ISSN 0092-8674