ArticleThe Journal of biological chemistry2010
Adipocyte fatty acid-binding protein modulates inflammatory responses in macrophages through a positive feedback loop involving c-Jun NH2-terminal kinases and activator protein-1.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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Who cites it
102 citing papers in PubMed, 186 citations in OpenAlex.
- Comprehensive Evaluation of Predictive Significance of FABP4 for Long-term Clinical Outcomes After Ischemic Stroke.Translational stroke research · 2026Trial
- Circulating adipocyte fatty acid-binding protein exacerbates LPS-induced neurotoxicity by crossing the disrupted blood-brain barrier and promoting neuronal apoptosis.Cell communication and signaling : CCS · 2026Article
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- Adipocyte fatty acid-binding protein 4 suppresses contraction of mouse ventricular myocytes via a calcium-independent pathway.Frontiers in physiology · 2026Article
- Inhibition of fatty acid-binding protein 4 alleviates psoriasis-like skin inflammation by modulating macrophage polarization.Frontiers in immunology · 2026Article
- Weight Loss-Associated Remodeling of Adipose Tissue Immunometabolism.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2025Review
- Fatty Acid-binding Protein 4 Exacerbates Blood-brain Barrier Disruption Through the JNK/c-Jun/MMP12 Pathway After Traumatic Brain Injury.Molecular neurobiology · 2025Article
- Intramuscular adipose tissue restricts functional muscle recovery.Cell reports · 2025Article
- New cardiovascular disease markers in patients with familial hypercholesterolemia carriers of genetic variants.Journal of diabetes and metabolic disorders · 2025Article
- Regulation of Blood-Brain Barrier Permeability via JNK Signaling Pathway: Mechanisms and Potential Therapeutic Strategies for Ischemic Stroke, Alzheimer's Disease and Brain Tumors.Molecules (Basel, Switzerland) · 2025Review
- Evaluation of the Anti-Inflammatory Effects of Novel Fatty Acid-Binding Protein 4 Inhibitors in Microglia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Immunometabolic reprogramming in macrophages infected with active and dormantInfection and immunity · 2025Article
- Extracellular vesicles in atherosclerosis cardiovascular disease: emerging roles and mechanisms.Frontiers in cardiovascular medicine · 2025Review
- Inhibition of the RXRA-PPARα-FABP4 signaling pathway alleviates vascular cellular aging by an SGLT2 inhibitor in an atherosclerotic mice model.Science China. Life sciences · 2024Article
- Activation of pregnane X receptor sensitizes alcoholic steatohepatitis by transactivating fatty acid binding protein 4.Acta pharmaceutica Sinica. B · 2024Article
- Time-Restricted Feeding Attenuates Adipose Tissue Inflammation and Fibrosis in Mice Under Chronic Light Exposure.International journal of molecular sciences · 2024Article
- Endothelial dysfunction: mechanisms and contribution to diseases.Acta pharmacologica Sinica · 2024Review
- Islet-Resident Memory T Cells Orchestrate the Immunopathogenesis of Type 1 Diabetes through the FABP4-CXCL10 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The Effects of FABP4 on Cardiovascular Disease in the Aging Population.Current atherosclerosis reports · 2024Review
42 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adipocyte fatty acid-binding protein (A-FABP) has emerged as an important mediator of inflammation in macrophages. Macrophage-selective ablation of A-FABP alone is sufficient to prevent the development of high cholesterol diet-induced atherosclerosis in apoE-deficient mice. However, the precise mechanisms whereby A-FABP modulates inflammation remain elusive. Here, we report that A-FABP forms a finely tuned positive loop between JNK and activator protein-1 (AP-1) to exacerbate lipopolysaccharide (LPS)-induced inflammatory responses in macrophages. Real time PCR and luciferase reporter analysis showed that LPS induced A-FABP expression through transcriptional activation. This effect was mediated by JNK, which promoted the recruitment of c-Jun to a highly conserved AP-1 consensus binding motif located within the proximal region of the A-FABP promoter. LPS-induced transactivation of the A-FABP gene was diminished by either pharmacological inhibition of JNK or knocking down c-Jun or by mutating the AP-1 recognition site within the proximal region (-122 to -116 bp) of the A-FABP promoter. Conversely, the LPS-evoked phosphorylation of JNK, activation of AP-1, and production of pro-inflammatory cytokines were markedly attenuated by pharmacological or genetic suppression of A-FABP in macrophages. Furthermore, the LPS-induced elevation in A-FABP expression could also be prevented by the selective A-FABP inhibitor BMS309403. These findings support the notion that pharmacological inhibition of A-FABP represents a valid strategy for treating inflammation-related disorders such as atherosclerosis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.