Mitochondrial fission promotes the continued clearance of apoptotic cells by macrophages
Open accessAbstract
Clearance of apoptotic cells (ACs) by phagocytes (efferocytosis) prevents post-apoptotic necrosis and dampens inflammation. Defective efferocytosis drives important diseases, including atherosclerosis. For efficient efferocytosis, phagocytes must be able to internalize multiple ACs. We show here that uptake of multiple ACs by macrophages requires dynamin-related protein 1 (Drp1)-mediated mitochondrial fission, which is triggered by AC uptake. When mitochondrial fission is disabled, AC-induced increase in cytosolic calcium is blunted owing to mitochondrial calcium sequestration, and calcium-dependent phagosome formation around secondarily encountered ACs is impaired. These defects can be corrected by silencing the mitochondrial calcium uniporter (MCU). Mice lacking myeloid Drp1 showed defective efferocytosis and its pathologic consequences in the thymus after dexamethasone treatment and in advanced atherosclerotic lesions in fat-fed Ldlr-/- mice. Thus, mitochondrial fission in response to AC uptake is a critical process that enables macrophages to clear multiple ACs and to avoid the pathologic consequences of defective efferocytosis in vivo.
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Sustainable clearance of multiple apoptotic cells by macrophages requires DRP1-mediated macrophage mitochondrial fission, allowing calcium release from mitochondria into cytoplasm, triggered by initial uptake of apoptotic cells.
“It is noteworthy that the sustainable clearance of multiple apoptotic cells by macrophages requires dynamin-related protein 1 (DRP1)-mediated macrophage mitochondrial fission, allowing calcium release from mitochondria into the cytoplasm, triggered by the initial uptake of apoptotic cells [147].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [147]
DRP1-deficient macrophages present impaired efferocytosis in vivo and subsequently increased plaque necrosis in advanced atherosclerotic lesions of Western diet-fed LDLR knockout mice.
“DRP1-deficient macrophages present impaired efferocytosis in vivo and subsequently increased plaque necrosis in advanced atherosclerotic lesions of Western diet-fed LDLR knockout mice [147].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [147]
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“To explain this observation, we considered whether preventing mitochondrial fission leads to defective LC3-associated phagocytosis (LAP), a process by which LC3-II conjugation to phagosomes enables phagosome-lysosome fusion and AC corpse degradation (Martinez et al., 2011; Martinez et al., 2016).”
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- Authors
- Wang, Y., Subramanian, M., Yurdagul, A., Barbosa-Lorenzi, V. C., Cai, B., de Juan-Sanz, J., Ryan, T. A., Nomura, M., Maxfield, F. R., & Tabas, I.
- Affiliations
- Columbia University (US)
- Institute of Genomics and Integrative Biology (IN)
- Weill Cornell Medicine (US)
- Kyushu University (JP)
- Columbia University Irving Medical Center (US)
- Corresponding author
- Tabas, Ira
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2017-10
- Volume
- 171
- Issue
- 2
- Pages
- 331-345.e22
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC5679712
- OpenAlex
- W2759443181
- Cited by
- 364
- References
- 50
- Citations by year
- 2026: 34 · 2025: 49 · 2024: 37 · 2023: 50 · 2022: 45 · 2021: 50 · 2020: 50 · 2019: 21 · 2018: 27 · 2017: 1
- FWCI
- 12.23
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Queen Mary Research Online (Queen Mary University of London) (submittedVersion)
- Columbia Academic Commons (Columbia University)
- Funders
- NIH/NIDDK (5P30DK063608)
- Office of the NIH Director under Shared Instrumentation (S10OD020056)
- American Heart Association (11PRE7450075)
- American Heart Association Post-Doctoral Fellowship (15POST25620024)
- KAKENHI (17K09885)
- Japanese Society for the Promotion of Science
- NIH (T32 HL007343-28, R37 NS036942, R01 HL093324, R01 HL075662, HL127464, HL132412)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- efferocytosis, mitochondrial fission, Drp1, macrophages, mitochondrial calcium uniporter, mitochondrial calcium sequestration, intracellular calcium, phagosome formation, atherosclerosis, thymus, inflammation
- MeSH terms
- Animals, Humans, Macrophages, Microtubule-Associated Proteins, Mitochondria, Phagocytes, Phagosomes, Apoptosis, Myeloid Cells, Mice, Mitochondrial Dynamics
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