@article{uneatlantico124,
            year = {2020},
           title = {A Network of Macrophages Supports Mitochondrial Homeostasis in the Heart},
         journal = {Cell},
          number = {1},
           month = {Octubre},
           pages = {94--109.e23},
          volume = {183},
          author = {Jos{\'e} A. Nicol{\'a}s-{\'A}vila and Ana V. Lechuga-Vieco and Lorena Esteban-Mart{\'i}nez and Mar{\'i}a S{\'a}nchez-D{\'i}az and Elena D{\'i}az-Garc{\'i}a and Demetrio J. Santiago and Andrea Rubio-Ponce and Jackson LiangYao Li and Akhila Balachander and Juan A. Quintana and Raquel Mart{\'i}nez-de-Mena and Beatriz Castej{\'o}n-Vega and Andr{\'e}s Pun-Garc{\'i}a and Paqui G. Trav{\'e}s and Elena Bonz{\'o}n-Kulichenko and Fernando Garc{\'i}a-Marqu{\'e}s and Lorena Cuss{\'o} and Noelia A-Gonz{\'a}lez and Andr{\'e}s Gonz{\'a}lez-Guerra and Marta Roche-Molina and Sandra Martin-Salamanca and Georgiana Crainiciuc and Gabriela Guzm{\'a}n and Jagoba Larrazabal and El{\'i}as Herrero-Gal{\'a}n and Jorge Alegre-Cebollada and Greg Lemke and Carla V. Rothlin and Luis Jes{\'u}s Jimenez-Borreguero and Guillermo Reyes and Antonio Castrillo and Manuel Desco and Pura Mu{\~n}oz-C{\'a}noves and Borja Ib{\'a}{\~n}ez and Miguel Torres and Lai Guan Ng and Silvia G. Priori and H{\'e}ctor Bueno and Jes{\'u}s V{\'a}zquez and Mario D. Cordero and Juan A. Bernal and Jos{\'e} A. Enr{\'i}quez and Andr{\'e}s Hidalgo},
        keywords = {Macrophage; Mitochondria; Autophagy; Proteostasis; Phagocytosis; Heart.},
             url = {http://repositorio.uneatlantico.es/id/eprint/124/},
        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.}
}