近日，西班牙CNIC研究所Andrés Hidalgo、José A. Enríquez等研究人员合作发现，巨噬细胞网络促进心脏线粒体的内稳态。该研究于2020年9月15日在线发表于《细胞》。

Title: A Network of Macrophages Supports Mitochondrial Homeostasis in the Heart

Author: José A. Nicolás-ávila, Ana V. Lechuga-Vieco, Lorena Esteban-Martínez, María Sánchez-Díaz, Elena Díaz-García, Demetrio J. Santiago, Andrea Rubio-Ponce, Jackson LiangYao Li, Akhila Balachander, Juan A. Quintana, Raquel Martínez-de-Mena, Beatriz Castejón-Vega, Andrés Pun-García, Paqui G. Través, Elena Bonzón-Kulichenko, Fernando García-Marqués, Lorena Cussó, Noelia A-González, Andrés González-Guerra, Marta Roche-Molina, Sandra Martin-Salamanca, Georgiana Crainiciuc, Gabriela Guzmán, Jagoba Larrazabal, Elías Herrero-Galán, Jorge Alegre-Cebollada, Greg Lemke, Carla V. Rothlin, Luis Jesús Jimenez-Borreguero, Guillermo Reyes, Antonio Castrillo, Manuel Desco, Pura Muoz-Cánoves, Borja Ibáez, Miguel Torres, Lai Guan Ng, Silvia G. Priori, Héctor Bueno, Jesús Vázquez, Mario D. Cordero, Juan A. Bernal, José A. Enríquez, Andrés Hidalgo

Issue&Volume: 2020-09-15

Abstract: Cardiomyocytes are subjected to the intense mechanical stress and metabolic demandsof the beating heart. It is unclear whether these cells, which are long-lived andrarely renew, manage to preserve homeostasis on their own. While analyzing macrophageslodged within the healthy myocardium, we discovered that they actively took up material,including mitochondria, derived from cardiomyocytes. Cardiomyocytes ejected dysfunctionalmitochondria and other cargo in dedicated membranous particles reminiscent of neuralexophers, through a process driven by the cardiomyocyte’s autophagy machinery thatwas enhanced during cardiac stress. Depletion of cardiac macrophages or deficiencyin the phagocytic receptor Mertk resulted in defective elimination of mitochondriafrom the myocardial tissue, activation of the inflammasome, impaired autophagy, accumulationof anomalous mitochondria in cardiomyocytes, metabolic alterations, and ventriculardysfunction. Thus, we identify an immune-parenchymal pair in the murine heart thatenables transfer of unfit material to preserve metabolic stability and organ function.

DOI: 10.1016/j.cell.2020.08.031

Source: https://www.cell.com/cell/fulltext/S0092-8674(20)31073-4