Journal
CELL
Volume 183, Issue 1, Pages 94-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2020.08.031
Keywords
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Categories
Funding
- Intramural grants from the Severo Ochoa program (IGP-SO)
- Ministerio de Ciencia - Innovacion (MICINN) [SAF2015-71878-REDT, SAF2014-56819-R]
- European Research Council [669387, 819775, ERC-741538]
- SIgN core funding from A*STAR
- Ministry of Science and Innovation [BFU2016-75144-R]
- (ISCIII) from MICINN [PGC2018-096486-B-I00, RD16/0011/0019]
- Leducq Foundation [TNE-17CVD04, TNE-18CVD04]
- Co-munidad de Madrid [S2017/BMD-3875]
- intramural grant TPC/O-SO
- HFSP [RGP0016/2018]
- intramural grant IGP-SO
- Carlos III Institute of Health [IPT17/0019-ISCIII-SGEFI/ERDF]
- Fondo de Investigaciones Sanitarias from MICINN [BIO2015-67580-P, PGC2018-097019-B-I00]
- MICINN [RTI2018-096068, SAF2015-65607-R, RTI2018-095497-B-I00, SVP-2014-068595, SVP-2013-068089, FJCI-2016-29384, BES-2016-076635, SEV-2015-0505]
- AFM
- MDA
- RENIM-CM from the Comunidad de Madrid [S2017/BMD-3867]
- European structural and investment funds
- Fundacio la Marato de TV3 [120/C/2015-20153032]
- La Caixa Foundation [HR17_00527]
- CNIC International Postdoctoral Program (EU grant) [600396]
- Pro-CNIC Foundation
- [SAF2015-65633-R]
- [RTI2018-099357-B-I00]
- [BIO2017-83640-P]
- [RYC-2014-16604]
- [LaCaixa-HR17-00040]
- [UPGRADE-H2020-825825]
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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.
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