ArticleBrain pathology (Zurich, Switzerland)2025
Potentiating microglial efferocytosis by MFG-E8 improves survival and neurological outcome after successful cardiopulmonary resuscitation in mice.
Article in Brain pathology (Zurich, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- ApoE impairs microglial efferocytosis by targeting Gas6/MerTK in a mouse model of acute seizure.Acta pharmacologica Sinica · 2026Article
- Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Macrophage efferocytosis promotes inflammation resolution and accelerates wound healing.Communications biology · 2026Review
- Lipid Metabolic Mediators Bridge Ischemic Heart Disease and Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2026Article
- Advancements in nanomedicine for the therapeutic regulation of efferocytosis: opportunities and challenges.Theranostics · 2026Review
- Impaired Efferocytosis of Pericytes and Vascular Smooth Muscle Cells in Diabetic Retinopathy.Cells · 2025Review
- Potentiating microglial efferocytosis by MFG-E8 improves survival and neurological outcome after successful cardiopulmonary resuscitation in mice.Brain pathology (Zurich, Switzerland) · 2025Article
- Microglia efferocytosis: an emerging mechanism for the resolution of neuroinflammation in Alzheimer's disease.Journal of neuroinflammation · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
Brain injury represents the leading cause of mortality and disability after cardiopulmonary resuscitation (CPR) from cardiac arrest (CA), in which the accumulation of dying cells aggravate tissue injury by releasing proinflammatory intracellular components. Microglia play an essential role in maintaining brain homeostasis via milk fat globule epidermal growth factor 8 (MFG-E8)-opsonized efferocytosis, the engulfment of dying cells and debris. This study investigates whether potentiating microglia efferocytosis by MFG-E8 provides neuroprotection after CA/CPR. After 8-minute asphyxial CA/CPR, male adult C57BL/6J mice were randomly assigned to receive recombinant mouse MFG-E8 (rmMFG-E8) or vehicle. We evaluated the survival and neurological deficits of mice, along with histological damages, phagocytosis index of dying cells, and microglia polarization. A transcriptome analysis was conducted to explore the downstream molecules modulated by MFG-E8. In mice resuscitated from CA, rmMFG-E8 administration significantly enhanced the efferocytosis of apoptotic cells by microglia, improved the survival and neurological function of mice, and attenuated neuropathological injuries. Additionally, rmMFG-E8 induced a prominent alteration in microglial gene expression and promoted a shift from a proinflammatory phenotype to an anti-inflammatory phenotype. Moreover, rmMFG-E8 treatment induced up-regulation of interferon regulatory factor 7 (IRF7), and IRF7 gene silencing largely reversed the neuroprotective effects of rmMFG-E8. This study demonstrates that rmMFG-E8 improves survival and neurological outcomes after CA/CPR by enhancing microglial efferocytosis and reshaping the inflammatory microenvironment in brain tissue. Potentiating MFG-E8 is a promising strategy to combat post-CA brain injury.
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Registered trials
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