ArticleArquivos brasileiros de cardiologia2026
Agonism of GPR84 Attenuates Free Fatty Acid-Induced Endothelial Inflammation and Monocyte Adhesion via Gfi1/NF-κB Pathway.
Article in Arquivos brasileiros de cardiologia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundEndothelial dysfunction and monocyte adhesion driven by free fatty acids (FFAs) are critical early events in atherosclerosis. Palmitate, a long-chain saturated free fatty acid, upregulated GPR84 expression. Although GPR84 is canonically activated by medium-chain FFAs, its induction under lipotoxic stress suggests a compensatory, context-dependent role. Its role in endothelial inflammation is poorly defined.
objectivesTo investigate the functional role of GPR84 activation in FFA-induced endothelial inflammation and elucidate the underlying mechanisms.
methodsHuman aortic endothelial cells (HAECs) were challenged with palmitate (0.5 or 1 mM) in the presence or absence of the GPR84 agonists 6-OAU or ZQ-16 (each at 1 μM). Inflammatory cytokine and adhesion molecule expression were assessed by qPCR and ELISA. Monocyte adhesion was evaluated using THP-1 cells. NF-κB p65 nuclear translocation and Gfi1 expression were examined, and Gfi1 silencing was performed to assess functional relevance.
resultsPalmitate increased GPR84 expression in HAECs. Treatment with GPR84 agonists significantly reduced palmitate-induced upregulation of IL-1β, TNF-α, MCP-1, VCAM-1, and ICAM-1 at both mRNA and protein levels, and attenuated THP-1 monocyte adhesion. Mechanistically, GPR84 activation inhibited NF-κB p65 nuclear translocation and preserved Gfi1 expression. Knockdown of Gfi1 abrogated the protective effects of GPR84 agonists, restoring NF-κB activation, adhesion molecule expression, and monocyte adhesion.
conclusionsGPR84 agonism mitigates FFA-induced endothelial inflammation by restoring Gfi1 expression and suppressing NF-κB signaling, highlighting a potential therapeutic strategy for early atherosclerosis that warrants further in vivo validation.
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