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探索GPR120/FFAR4药理学：通过分子信号通路揭示阿尔茨海默病干预的新治疗途径。

Exploring GPR120/FFAR4 pharmacology: Unveiling novel therapeutic avenues through molecular signaling pathways for Alzheimer's disease intervention.

作者信息

Gogu Priyadharshini, Bharti Jayhind, Yadav Jagat Pal, Grishina Maria, Verma Amita, Kumar Vikas, Singh Ankit Kumar, Verma Akash, Kumar Pradeep, Khalilullah Habibullah, Jaremko Mariusz, Emwas Abdul-Hamid, Dwivedi Ashish R, Pathak Prateek

机构信息

Laboratory of Drug Discovery, School of Pharmacy, GITAM (Deemed to be University), 502239, India.

Bioorganic and Medicinal Chemistry Research Laboratory, School of Pharmacy, Sam Higginbottam Institute of Agriculture, Technology and Sciences, 211007, India.

出版信息

Brain Behav Immun Health. 2025 Jul 11;48:101061. doi: 10.1016/j.bbih.2025.101061. eCollection 2025 Oct.

DOI:10.1016/j.bbih.2025.101061
PMID:40697975
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12281026/
Abstract

G-protein-coupled receptors (GPCRs) are a major class of membrane proteins involved in numerous physiological and pathological processes. Among them, free fatty acid receptor 4 (FFAR4/GPR120), activated by long-chain free fatty acids, has shown anti-inflammatory effects and is expressed in the brain-implicating its role in neurodegenerative diseases like Alzheimer's disease (AD). AD is characterized by brain atrophy, cognitive decline, and neuroinflammation, involving complex signaling networks. This review explores the pharmacological relevance of GPR120/FFAR4 in AD, focusing on its involvement in neuroinflammatory, amyloidogenic, and intracellular signaling cascades. Targeting GPR120 may help modulate chronic inflammation and amyloid-β accumulation. Additionally, activation of nuclear receptors and regulation of pathways such as MAPK, NLRP3, PPARs, and cAMP have shown promise in mitigating AD pathology. Despite the complexity of brain signaling, GPR120 emerges as a compelling multitarget therapeutic receptor. These insights provide a foundation for developing novel anti-inflammatory strategies in AD treatment.

摘要

G蛋白偶联受体（GPCRs）是一类主要的膜蛋白，参与众多生理和病理过程。其中，游离脂肪酸受体4（FFAR4/GPR120）由长链游离脂肪酸激活，已显示出抗炎作用，且在大脑中表达，这暗示了其在诸如阿尔茨海默病（AD）等神经退行性疾病中的作用。AD的特征是脑萎缩、认知衰退和神经炎症，涉及复杂的信号网络。本综述探讨了GPR120/FFAR4在AD中的药理学相关性，重点关注其在神经炎症、淀粉样蛋白生成和细胞内信号级联反应中的作用。靶向GPR120可能有助于调节慢性炎症和β淀粉样蛋白的积累。此外，激活核受体以及调节丝裂原活化蛋白激酶（MAPK）、NOD样受体蛋白3（NLRP3）、过氧化物酶体增殖物激活受体（PPARs）和环磷酸腺苷（cAMP）等信号通路在减轻AD病理方面已显示出前景。尽管大脑信号传导复杂，但GPR120成为一种引人注目的多靶点治疗受体。这些见解为开发AD治疗中的新型抗炎策略奠定了基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/deb0774a3cc1/gr11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/00956c6253ac/gr1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/43d3c9ef3979/gr4.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/8ee6bc54a6cc/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/220ac588f3bb/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/deb0774a3cc1/gr11.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/00956c6253ac/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/f8ebf49164cf/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/2e52420bd9b3/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/43d3c9ef3979/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/e55f425c129d/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/c8e4b8adc981/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/858fdad9e25c/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/43a4073280b4/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/8ee6bc54a6cc/gr9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/220ac588f3bb/gr10.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/216d/12281026/deb0774a3cc1/gr11.jpg

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本文引用的文献

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Mol Biomed. 2024 Apr 22;5(1):14. doi: 10.1186/s43556-024-00179-x.
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Positive interplay between FFAR4/GPR120, DPP-IV inhibition and GLP-1 in beta cell proliferation and glucose homeostasis in obese high fat fed mice.肥胖高脂喂养小鼠中 FFAR4/GPR120、DPP-IV 抑制与 GLP-1 之间的正相互作用在β细胞增殖和葡萄糖稳态中的作用。
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