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00925njm 22002777a 4500 dc Nicolas-Avila, Jose A. author Lechuga-Vieco, Ana V. author Esteban-Martinez, Lorena author Sanchez-Diaz, Maria author Díaz-García, Elena author Santiago, Demetrio J author Rubio-Ponce, Andrea author Li, Jackson LiangYao author Balachander, Akhila author Quintana, Juan A. author Martínez-de-Mena, Raquel author Castejón-Vega, Beatriz author Pun-Garcia, Andres author Través, Paqui G author Bonzon-Kulichenko, Elena author Garcia-Marques, Fernando author Cusso, Lorena author Alonso-Gonzalez, Noelia author González-Guerra, Andrés author Roche-Molina, Marta author Martin-Salamanca, Sandra author Crainiciuc, Georgiana author Guzman-Martinez, Gabriela author Larrazabal, Jagoba author Herrero-Galan, Elas author Alegre-Cebollada, Jorge author Lemke, Greg author Rothlin, Carla V author Jimenez-Borreguero, Luis J. author Reyes, Guillermo author Castrillo, Antonio author Desco, Manuel author Munoz-Canoves, Pura author Ibáñez, Borja author Torres, Miguel author Ng, Lai Guan author Priori, Silvia G. author Bueno, Hector author Vazquez, Jesus author Cordero, Mario D author Bernal, Juan Antonio author Enriquez, Jose Antonio author Hidalgo, Andres author 2020-10-01 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. VIDEO ABSTRACT. Cell. 2020; 183(1):94-109 10.1016/j.cell.2020.08.031 0092-8674 Cell 32937105 http://hdl.handle.net/20.500.12105/11210 A Network of Macrophages Supports Mitochondrial Homeostasis in the Heart.