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Metabolic Characterization of Polarized M1 and M2 Bone Marrow-derived Macrophages Using Real-time Extracellular Flux Analysis
Published on: November 28, 2015
Mitochondrial metabolic reprogramming, quality control, and intercellular transfer in regulating macrophage
1Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.
Frontiers in Physiology
|May 18, 2026
Summary
Macrophage metabolism dictates immune responses, with distinct pathways like glycolysis and oxidative phosphorylation (OXPHOS) driving M1 and M2 polarization. Understanding these metabolic shifts, including mitochondrial roles and intercellular transfer, offers new therapeutic targets.
Area of Science:
- Immunometabolism
- Mitochondrial Biology
- Cellular Signaling
Background:
- Macrophage function is plastic and tightly regulated by metabolic reprogramming.
- Mitochondria are crucial for energy, metabolic intermediates, and reactive oxygen species (ROS) signaling in macrophages.
- Distinct metabolic states, M1 (glycolysis) and M2 (OXPHOS), characterize macrophage polarization.
Purpose of the Study:
- To review the metabolic paradigms of M1 and M2 macrophage polarization.
- To highlight molecular mechanisms linking metabolism to inflammation, such as TCA cycle truncation and succinate accumulation.
- To discuss mitochondrial quality control and intercellular mitochondrial transfer in macrophage homeostasis and immune regulation.
Main Methods:
- Literature review focusing on immunometabolism and macrophage biology.
- Analysis of molecular mechanisms driving macrophage polarization.
- Synthesis of recent findings on mitochondrial dynamics, mitophagy, and intercellular mitochondrial transfer.
Main Results:
- Macrophage polarization is associated with distinct metabolic profiles: M1 macrophages favor glycolysis, while M2 macrophages rely on oxidative phosphorylation (OXPHOS).
- Tricarboxylic acid (TCA) cycle truncation and succinate accumulation are key metabolic events promoting inflammatory M1 polarization.
- Mitochondrial quality control (dynamics, mitophagy) and intercellular mitochondrial transfer are critical for maintaining macrophage function and regulating the immune microenvironment.
Conclusions:
- Metabolic reprogramming, particularly mitochondrial function and substrate utilization, is central to macrophage plasticity and immune responses.
- Targeting macrophage metabolism, including mitochondrial pathways and intercellular transfer, presents novel opportunities for metabolic immunotherapy in inflammatory diseases, cancer, and sepsis.
- Macrophage metabolic and mitochondrial regulation is highly context-dependent, varying across tissues and disease states.
