Fatty acid metabolism and lipid channeling in macrophages: mechanisms of inflammation, resolution, and lipotoxicity
- 1Department of Microbiology and Immunology, Louisiana State University Health Sciences Center
- 2Center for Applied Immunology and Pathological Processes (CAIPP), Louisiana State University Health Sciences Center
Abstract
Macrophages integrate metabolic signals with immune activation, and their ability to handle fatty acids is central to preventing lipotoxicity and to sustaining effector functions. In cardiometabolic settings such as obesity, metabolic dysfunction-associated steatotic liver disease, and atherosclerosis, chronic exposure to excess free fatty acids and toxic lipid species, such as ceramides, disrupts organelle integrity, impairs efferocytosis, and skews macrophages toward pro-inflammatory phenotypes. This review examines how macrophages channel fatty acids into β-oxidation, glycerolipid synthesis and storage, sphingolipid production, and polyunsaturated fatty acid-derived lipid mediator biosynthesis to shape the balance among metabolic adaptation, inflammatory activation, resolution, and lipid-induced dysfunction. We also highlight lipin-1 as a regulatory node at a key branchpoint in macrophage lipid metabolism. By linking glycerolipid synthesis, lipid storage, mitochondrial metabolism, and inflammatory signaling, lipin-1 illustrates how lipid routing can influence macrophage function in cardiometabolic disease.
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BibTeX
@article{bamgbose2026fatty,
title = {{Fatty acid metabolism and lipid channeling in macrophages: mechanisms of inflammation, resolution, and lipotoxicity}},
author = {Temitayo T. Bamgbose and Oluwakemi Osarumwense Igiehon and Javier Nión Fieira and Cora Palmer and Andrii Andriichuk and Matthew D. Woolard},
journal = {Frontiers in Immunology},
year = {2026},
month = jun,
doi = {10.3389/fimmu.2026.1839069},
url = {https://doi.org/10.3389/fimmu.2026.1839069},
note = {CC BY},
}
RIS
TY - JOUR
TI - Fatty acid metabolism and lipid channeling in macrophages: mechanisms of inflammation, resolution, and lipotoxicity
AU - Temitayo T. Bamgbose
AU - Oluwakemi Osarumwense Igiehon
AU - Javier Nión Fieira
AU - Cora Palmer
AU - Andrii Andriichuk
AU - Matthew D. Woolard
PY - 2026
DA - 2026/06/12
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1839069
UR - https://doi.org/10.3389/fimmu.2026.1839069
AB - Macrophages integrate metabolic signals with immune activation, and their ability to handle fatty acids is central to preventing lipotoxicity and to sustaining effector functions. In cardiometabolic settings such as obesity, metabolic dysfunction-associated steatotic liver disease, and atherosclerosis, chronic exposure to excess free fatty acids and toxic lipid species, such as ceramides, disrupts organelle integrity, impairs efferocytosis, and skews macrophages toward pro-inflammatory phenotypes. This review examines how macrophages channel fatty acids into β-oxidation, glycerolipid synthesis and storage, sphingolipid production, and polyunsaturated fatty acid-derived lipid mediator biosynthesis to shape the balance among metabolic adaptation, inflammatory activation, resolution, and lipid-induced dysfunction. We also highlight lipin-1 as a regulatory node at a key branchpoint in macrophage lipid metabolism. By linking glycerolipid synthesis, lipid storage, mitochondrial metabolism, and inflammatory signaling, lipin-1 illustrates how lipid routing can influence macrophage function in cardiometabolic disease.
SN - 1664-3224
ER -