Fgr kinase is required for proinflammatory macrophage activation during diet-induced obesity
Open accessAbstract
Proinflammatory macrophages are key in the development of obesity. In addition, reactive oxygen species (ROS), which activate the Fgr tyrosine kinase, also contribute to obesity. Here we show that ablation of Fgr impairs proinflammatory macrophage polarization while preventing high-fat diet (HFD)-induced obesity in mice. Systemic ablation of Fgr increases lipolysis and liver fatty acid oxidation, thereby avoiding steatosis. Knockout of Fgr in bone marrow (BM)-derived cells is sufficient to protect against insulin resistance and liver steatosis following HFD feeding, while the transfer of Fgr-expressing BM-derived cells reverts protection from HFD feeding in Fgr-deficient hosts. Scavenging of mitochondrial peroxides is sufficient to prevent Fgr activation in BM-derived cells and HFD-induced obesity. Moreover, Fgr expression is higher in proinflammatory macrophages and correlates with obesity traits in both mice and humans. Thus, our findings reveal the mitochondrial ROS-Fgr kinase as a key regulatory axis in proinflammatory adipose tissue macrophage activation, diet-induced obesity, insulin resistance and liver steatosis.
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In the context of obesity, matrix mtROS and not Nox2-derived ROS were crucial for activation of FGR.
“In contrast to the study by Garaude et al., matrix mtROS and not Nox2-derived ROS were crucial for activation of FGR, supporting the observation of other studies that ROS have to be produced in direct vicinity of the regulated target and do not excessively saturate the cell until they hit their target at random [29,30,37,61,125,273].”
From Functions of ROS in Macrophages and Antimicrobial Immunity (2021) · cites this paper as [272]
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“The absence of Fgr leads to increased FAO and decreased lipid droplet accumulation after exposure to pathogen-associated molecular patterns (96).”
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BackgroundA Model for the Signal Initiation Complex Between Arrestin-3 and the Src Family Kinase Fgr
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Research Progress Into Adipose Tissue Macrophages and Insulin Resistance
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Inflammation macrophages contribute to cardiac homeostasis
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Role of Natural Antioxidants in Cancer
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“adipose inflammation and metabolic dysfunction caused by M1 polarization of adipocyte macrophages in diet induced obesity (Acín-Pérez et al., 2020).”
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“The increase in CII activity is also required for pro-in fl ammatory macrophage-dependent host defense (Garaude et al., 2016) and diet-induced obesity (Acín-Pérez et al., 2020).”
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“These metabolic insults contribute to hallmark features of CKM, including insulin resistance, endothelial dysfunction, and renal injury [30–34].”
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“It has been reported that the loss of FGR inhibits the pro-inflammatory M1 MΦ polarization while enhancing the anti-inflammatory M2 MΦ polarization [68].”
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“54 infiltration.”
Adropin deficiency worsens TNBS-induced colitis
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“52 Next, our PathfindR KEGG analyses suggested overrepre-sentation of hypoxia-responsive (HIF-1 pathways) and mitochondrial oxidative phosphorylation pathways in SAT in relation to plasma triglycerides.”
Looking Back to the Future of Mitochondrial Research
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“, 2020), in metabolic reprogramming of macrophages (Mills et al., 2016; Acín-Pérez et al., 2020), in angiogenesis (Herkenne et al.”
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Conservation and divergence in the allosteric architectures of five human protein kinasesPreprint
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“FGR is a myeloid-restricted SRC-family kinase active in neutrophils, monocytes and macrophages, where it participates in integrin-dependent activation and inflammation 30,31 , and regulates mitochondrial complex II activity to support metabolic adaptation 32 .”
Systems approach identifies monocyte imbalance in symptomatic and asymptomatic P. vivax malaria
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“4D,E, including SPI1 , implicated in monocytic autophagy (Xie et al, 2023) and FGR , encoding a monocytes tyrosine kinase (Hatakeyama et al, 1996) with pro-in fl ammatory action (Acin-Perez et al, 2020), were also downregulated during asymptomatic P. vivax infections (Fig.”
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“Critically, our data demonstrates that the Fgr-STAT3 signaling pathway contributes to neuroinflammation and Fgr, a crucial member of the Src family of non-receptor tyrosine kinases, regulates macrophage-and neutrophil-mediated inflammatory responses [11, 34].”
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Sex-specific genetic regulation of adipose mitochondria and metabolic syndrome by Ndufv2
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The Function Mechanism of Weight Loss Drugs and New Research Progress in Weight Loss
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“DGE analysis in the Ccr2+MP in the aged hearts revealed upregulation of genes such as Fgr and Myof1 ( Supplementary Table 3 ), which have previously been linked to a pro-inflammatory phenotype 42,43 .”
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“Unlike mPTP-dependent RIRR, FGR-RIRR does not require pore opening, targets a metabolic enzyme rather than pore-forming proteins and maintains, or even hyperpolarizes, initial ΔΨ mt while reorienting electron flux [192].”
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- Authors
- Acín-Pérez, R., Iborra, S., Martí-Mateos, Y., Cook, E. C. L., Conde-Garrosa, R., Petcherski, A., Muñoz, M. D. M., Martínez de Mena, R., Krishnan, K. C., Jiménez, C., Bolaños, J. P., Laakso, M., Lusis, A. J., Shirihai, O. S., Sancho, D., & Enríquez, J. A.
- Affiliations
- Universidad Complutense de Madrid (ES)
- Spanish National Centre for Cardiovascular Research (ES)
- University of California, Los Angeles (US)
- Consejo Superior de Investigaciones Científicas (ES)
- University of Eastern Finland (FI)
- Corresponding author
- Sancho, David
- ORCID
- Venue
- Nature Metabolism
- Published
- 2020-09-17
- Volume
- 2
- Issue
- 9
- Pages
- 974-988
- ISSN
- 2522-5812 (ISSN-L)
- PMC
- PMC8225238
- OpenAlex
- W3087729805
- Cited by
- 83
- References
- 51
- Citations by year
- 2026: 12 · 2025: 18 · 2024: 11 · 2023: 12 · 2022: 12 · 2021: 18
- FWCI
- 7.53
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- DIGITAL.CSIC (Spanish National Research Council (CSIC)) (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institute on Aging (R21AG060456, R21AG063373)
- National Heart, Lung, and Blood Institute (P01HL028481)
- National Cancer Institute (R01CA232056)
- National Institute of Diabetes and Digestive and Kidney Diseases (R00DK120875, K99DK120875, R01DK099618, R01DK117850)
- Topics
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Keywords
- inflammatory macrophages, diet-induced obesity, high-fat diet, macrophage polarization, reactive oxygen species, electron transport chain, insulin resistance, hepatic steatosis, lipolysis, fatty acid oxidation, adipose tissue macrophages, bone marrow-derived cells, cellular bioenergetics
- MeSH terms
- Animals, Bone Marrow Cells, Fatty Liver, Inflammation, Insulin Resistance, Macrophage Activation, Magnetic Resonance Imaging, Mice, Inbred C57BL, Mitochondria, Liver, Obesity, Proto-Oncogene Proteins, Reactive Oxygen Species, Mice, Knockout, src-Family Kinases, Adipose Tissue, White, Interleukin-1beta, Diet, High-Fat
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