Efferocytosis-induced lactate enables the proliferation of pro-resolving macrophages to mediate tissue repair.


Journal

Nature metabolism
ISSN: 2522-5812
Titre abrégé: Nat Metab
Pays: Germany
ID NLM: 101736592

Informations de publication

Date de publication:
27 Nov 2023
Historique:
received: 15 05 2023
accepted: 05 10 2023
medline: 28 11 2023
pubmed: 28 11 2023
entrez: 27 11 2023
Statut: aheadofprint

Résumé

The clearance of apoptotic cells by macrophages (efferocytosis) prevents necrosis and inflammation and activates pro-resolving pathways, including continual efferocytosis. A key resolution process in vivo is efferocytosis-induced macrophage proliferation (EIMP), in which apoptotic cell-derived nucleotides trigger Myc-mediated proliferation of pro-resolving macrophages. Here we show that EIMP requires a second input that is integrated with cellular metabolism, notably efferocytosis-induced lactate production. Lactate signalling via GPR132 promotes Myc protein stabilization and subsequent macrophage proliferation. This mechanism is validated in vivo using a mouse model of dexamethasone-induced thymocyte apoptosis, which elevates apoptotic cell burden and requires efferocytosis to prevent inflammation and necrosis. Thus, EIMP, a key process in tissue resolution, requires inputs from two independent processes: a signalling pathway induced by apoptotic cell-derived nucleotides and a cellular metabolism pathway involving lactate production. These findings illustrate how seemingly distinct pathways in efferocytosing macrophages are integrated to carry out a key process in tissue resolution.

Identifiants

pubmed: 38012414
doi: 10.1038/s42255-023-00921-9
pii: 10.1038/s42255-023-00921-9
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : U.S. Department of Health & Human Services | National Institutes of Health (NIH)
ID : R35-HL145228
Organisme : American Heart Association (American Heart Association, Inc.)
ID : 900337

Informations de copyright

© 2023. The Author(s), under exclusive licence to Springer Nature Limited.

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Auteurs

David Ngai (D)

Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA. dhn2111@columbia.edu.

Maaike Schilperoort (M)

Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA.

Ira Tabas (I)

Department of Medicine, Columbia University Irving Medical Center, New York, NY, USA. iat1@columbia.edu.
Departments of Physiology and Cell Biology, Columbia University Irving Medical Center, New York, NY, USA. iat1@columbia.edu.

Classifications MeSH