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, crosstalk between cardiac macrophages and cardiomyocytes is vital for maintaining electrical stability and metabolic homeostasis through the efferocytosis of damaged mitochondria.
“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]
The Summary (p. 2) reports that cardiac macrophages take up cardiomyocyte-derived mitochondria and help preserve metabolic stability in the murine heart. The Discussion (p. 13) treats electrical conductance as a separate, previously reported role; it does not establish that disposal of damaged mitochondria maintains electrical stability. (LLM, conf=0.88)
Experimental — accuracy not yet measuredImpaired macrophage-mediated clearance of damaged mitochondria can exacerbate cardiomyocyte dysfunction.
“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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- 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
- Health Sciences › Medicine › Epidemiology › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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