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A Network of Macrophages Supports Mitochondrial Homeostasis in the Heart
Open accessAbstract
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.
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“Under physiological conditions, this crosstalk is vital for maintaining electrical stability and metabolic homeostasis through the efferocytosis of damaged mitochondria [11,12].”
From Cardiac Macrophages Exhibit Dynamic Heterogeneity and Functional Specialization During Experimental Autoimmune Myocarditis. (2026) · cites this paper as [12]
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“This aligns with previous reports indicating that impaired macrophage-mediated clearance of damaged mitochondria can exacerbate cardiomyocyte dysfunction [12].”
From Cardiac Macrophages Exhibit Dynamic Heterogeneity and Functional Specialization During Experimental Autoimmune Myocarditis. (2026) · cites this paper as [12]
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Metadata
- Authors
- Nicolás-Ávila, J. A., Lechuga-Vieco, A. V., Esteban-Martínez, L., Sánchez-Díaz, M., Díaz-García, E., Santiago, D. J., Rubio-Ponce, A., Li, J. L., Balachander, A., Quintana, J. A., Martínez-de-Mena, R., Castejón-Vega, B., Pun-García, A., Través, P. G., Bonzón-Kulichenko, E., García-Marqués, F., Cussó, L., A-González, N., González-Guerra, A., Roche-Molina, M., Martin-Salamanca, S., Crainiciuc, G., Guzmán, G., Larrazabal, J., Herrero-Galán, E., Alegre-Cebollada, J., Lemke, G., Rothlin, C. V., Jimenez-Borreguero, L. J., Reyes, G., Castrillo, A., Desco, M., Muñoz-Cánoves, P., Ibáñez, B., Torres, M., Ng, L. G., Priori, S. G., Bueno, H., Vázquez, J., Cordero, M. D., Bernal, J. A., Enríquez, J. A., & Hidalgo, A.
- Affiliations
- Spanish National Centre for Cardiovascular Research (ES)
- Agency for Science, Technology and Research (SG)
- Salk Institute for Biological Studies (US)
- University of Münster (DE)
- Hospital Universitario La Paz (ES)
- Yale University (US)
- Hospital Universitario de La Princesa (ES)
- Universidad de Las Palmas de Gran Canaria (ES)
- University of Pavia (IT)
- Universidad Europea del Atlántico (ES)
- Corresponding author
- Hidalgo, Andrés
- ORCID
- Esteban-Martínez, Lorena
- Sánchez-Díaz, María
- Santiago, Demetrio J.
- Rubio-Ponce, Andrea
- Li, Jackson LiangYao
- Balachander, Akhila
- Través, Paqui G.
- García-Marqués, Fernando
- Cussó, Lorena
- A-González, Noelia
- González-Guerra, Andrés
- Roche-Molina, Marta
- Crainiciuc, Georgiana
- Guzmán, Gabriela
- Herrero-Galán, Elías
- Alegre-Cebollada, Jorge
- Lemke, Greg
- Rothlin, Carla V.
- Reyes, Guillermo
- Castrillo, Antonio
- Desco, Manuel
- Ibáñez, Borja
- Torres, Miguel
- Ng, Lai Guan
- Priori, Silvia G.
- Bueno, Héctor
- Vázquez, Jesús
- Cordero, Mario D.
- Bernal, Juan A.
- Enríquez, José A.
- Hidalgo, Andrés
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2020-10
- Volume
- 183
- Issue
- 1
- Pages
- 94-109.e23
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W3086660393
- Cited by
- 762
- References
- 61
- Citations by year
- 2026: 136 · 2025: 144 · 2024: 147 · 2023: 131 · 2022: 101 · 2021: 89 · 2020: 14
- FWCI
- 60.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Zenodo (CERN European Organization for Nuclear Research) (submittedVersion, cc-by)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion, cc-by-sa)
- RUIdeRA - Institutional University Repository (University of Castilla-La Mancha) (submittedVersion, other-oa)
- Funders
- Instituto de Salud Carlos III
- Cordis (UPGRADE-H2020-825825)
- Ministerio de Economía y Competitividad (RYC-2014-16604)
- Association Française contre les Myopathies
- “la Caixa” Foundation (LaCaixa-HR17-00040)
- Fundació la Marató de TV3 (HR17_00527, 120/C/2015-20153032)
- European Research Council (ERC-COG-2018-ID, 819775, ERC-ADG-2014-ID:669387, ERC-741538)
- Fondation Leducq (TNE-17CVD04, TNE-18CVD04)
- Human Frontier Science Program (IPT17/0019-ISCIII-SGEFI/ERDF, RGP0016/2018)
- Centro Nacional de Investigaciones Cardiovasculares
- Howard Hughes Medical Institute (600396)
- Agency for Science, Technology and Research (BFU2016-75144-R)
- Ministerio de Ciencia e Innovación (SAF2015-71878-REDT, SAF2014-56819-R, FJCI-2016-29384, SAF2015-65633-R, PGC2018-096486-B-I00, BIO2015-67580-P, SAF2015-65607-R, BES-2016-076635, SVP-2014-068595, RD16/0011/0019, PGC2018-097019-B-I00, RTI2018-095497-B-I00, SVP-2013-068089, BIO2017-83640-P, RTI2018-099357-B-I00, SEV-2015-0505, RTI2018-096068)
- Muscular Dystrophy Association (ERC-741538)
- Comunidad de Madrid (S2017/BMD-3875, S2017/BMD-3867 RENIM-CM)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- cardiac macrophages, mitochondrial homeostasis, cardiomyocytes, mitochondrial transfer, autophagy, MERTK, phagocytosis, inflammasome, cardiac stress, ventricular dysfunction, myocardium
- MeSH terms
- c-Mer Tyrosine Kinase, Aged, Animals, Autophagy, Female, Heart, Homeostasis, Humans, Macrophages, Male, Mice, Inbred C57BL, Middle Aged, Mitochondria, Myocardial Infarction, Myocardium, Phagocytosis, Apoptosis, Reactive Oxygen Species, Receptor Protein-Tyrosine Kinases, Myocytes, Cardiac, Mice
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