The article explores the multifaceted roles of succinate in inflammation, particularly its function as a signaling molecule within immune responses. Succinate, a tricarboxylic acid (TCA) cycle intermediate, is produced from α-ketoglutarate and can accumulate under conditions of hypoxia or anaerobic glycolysis. This accumulation leads to the stabilization of hypoxia-inducible factor-1α (HIF-1α) and the generation of reactive oxygen species (ROS), contributing to pro-inflammatory processes. The article discusses how succinate acts as a signaling molecule through the activation of the succinate receptor 1 (SUCNR1), a G protein-coupled receptor. SUCNR1 is expressed in various immune cells and tissues, and its activation can either amplify or modulate inflammatory responses, depending on the context. The article also reviews the therapeutic potential of targeting succinate metabolism and SUCNR1 in inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, obesity, and atherosclerosis. Pharmacological interventions, including enzyme inhibitors and SUCNR1 antagonists, are discussed as potential strategies to modulate succinate levels and reduce inflammation. The authors highlight the need for further research to fully understand the complex roles of succinate and its receptor in inflammation and to develop effective therapeutic approaches.The article explores the multifaceted roles of succinate in inflammation, particularly its function as a signaling molecule within immune responses. Succinate, a tricarboxylic acid (TCA) cycle intermediate, is produced from α-ketoglutarate and can accumulate under conditions of hypoxia or anaerobic glycolysis. This accumulation leads to the stabilization of hypoxia-inducible factor-1α (HIF-1α) and the generation of reactive oxygen species (ROS), contributing to pro-inflammatory processes. The article discusses how succinate acts as a signaling molecule through the activation of the succinate receptor 1 (SUCNR1), a G protein-coupled receptor. SUCNR1 is expressed in various immune cells and tissues, and its activation can either amplify or modulate inflammatory responses, depending on the context. The article also reviews the therapeutic potential of targeting succinate metabolism and SUCNR1 in inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, obesity, and atherosclerosis. Pharmacological interventions, including enzyme inhibitors and SUCNR1 antagonists, are discussed as potential strategies to modulate succinate levels and reduce inflammation. The authors highlight the need for further research to fully understand the complex roles of succinate and its receptor in inflammation and to develop effective therapeutic approaches.