Anti-Atherosclerotic Potential of Free Fatty Acid Receptor 4 (FFAR4)
Autor: | Kamila Stachyra, Rafał Olszanecki, Anna Kiepura |
---|---|
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Cell signaling QH301-705.5 Medicine (miscellaneous) Inflammation Stimulation Review 030204 cardiovascular system & hematology GPR132 General Biochemistry Genetics and Molecular Biology liver steatosis 03 medical and health sciences 0302 clinical medicine FFAR4 Free fatty acid receptor 1 medicine Biology (General) Receptor Chemistry GPR120 free fatty acid receptors macrophages GPR31 030104 developmental biology Biochemistry inflammation medicine.symptom atherosclerosis apoE-knockout mice |
Zdroj: | Biomedicines Biomedicines, Vol 9, Iss 467, p 467 (2021) |
ISSN: | 2227-9059 |
Popis: | Fatty acids (FAs) are considered not only as a basic nutrient, but are also recognized as signaling molecules acting on various types of receptors. The receptors activated by FAs include the family of rhodopsin-like receptors: GPR40 (FFAR1), GPR41 (FFAR3), GPR43 (FFAR2), GPR120 (FFAR4), and several other, less characterized G-protein coupled receptors (GPR84, GPR109A, GPR170, GPR31, GPR132, GPR119, and Olfr78). The ubiquitously distributed FFAR4 can be activated by saturated and unsaturated medium- and long-chain fatty acids (MCFAs and LCFAs), as well as by several synthetic agonists (e.g., TUG-891). The stimulation of FFAR4 using selective synthetic agonists proved to be promising strategy of reduction of inflammatory reactions in various tissues. In this paper, we summarize the evidence showing the mechanisms of the potential beneficial effects of FFAR4 stimulation in atherosclerosis. Based partly on our own results, we also suggest that an important mechanism of such activity may be the modulatory influence of FFAR4 on the phenotype of macrophage involved in atherogenesis. |
Databáze: | OpenAIRE |
Externí odkaz: |