ReviewEndocrinology2021
FFAR4: A New Player in Cardiometabolic Disease?
Review in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- FFAR4 Mediates High-Altitude Hypoxia-Induced Asthenozoospermia through Oxidative Stress and Mitochondrial Dysfunction: An Integrative Bioinformatics and Experimental Study.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Comparative Transcriptomic Analysis of Human Macrophages During Mycobacterium avium Versus Mycobacterium tuberculosis Infection.Molecular microbiology · 2026Article
- Podocyte FFAR4 deficiency aggravated glomerular diseases and aging.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- G-protein coupled receptors in metabolic reprogramming and cancer.Pharmacology & therapeutics · 2025Review
- FFAR4 Deficiency Increases Necrotic Cores in Advanced Lesions of ApoEArteriosclerosis, thrombosis, and vascular biology · 2025Article
- The cardioprotective role of the G protein-coupled receptor FFAR4 in atherosclerosis is independent of macrophage foam cell regulation.The Journal of biological chemistry · 2025Article
- Potential Therapeutic Exploitation of G Protein-Coupled Receptor 120 (GPR120/FFAR4) Signaling in Obesity-Related Metabolic Disorders.International journal of molecular sciences · 2025Review
- GPR120/FFAR4 protects retinal vascular endothelial cells against high glucose injuryInternational journal of ophthalmology · 2025Article
- G protein-coupled receptors and traditional Chinese medicine: new thinks for the development of traditional Chinese medicine.Chinese medicine · 2024Review
- Spaceflight induces changes in gene expression profiles linked to insulin and estrogen.Communications biology · 2024Article
- Current Insights into the Effects of Dietary α-Linolenic Acid Focusing on Alterations of Polyunsaturated Fatty Acid Profiles in Metabolic Syndrome.International journal of molecular sciences · 2024Review
- New Insights in the Control of Fat Homeostasis: The Role of Neurotensin.International journal of molecular sciences · 2022Review
- Review
- Identification of Immune-Cell-Related Prognostic Biomarkers of Esophageal Squamous Cell Carcinoma Based on Tumor Microenvironment.Frontiers in oncology · 2021Article
- How important are fatty acids in human health and can they be used in treating diseases?Gut microbesReview
- Curcumin Derivative MTH-3 Regulates Palmitate-induced Insulin Resistance in Mouse Myoblast CIn vivo (Athens, Greece)Article
Corrections and comments
- Commented on by
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Free fatty acids (FFAs) are implicated in the pathogenesis of metabolic diseases that includes obesity, type 2 diabetes mellitus, and cardiovascular disease (CVD). FFAs serve as ligands for free fatty acid receptors (FFARs) that belong to the family of rhodopsin-like G protein-coupled receptors (GPCRs) and are expressed throughout the body to maintain energy homeostasis under changing nutritional conditions. Free fatty acid receptor 4 (FFAR4), also known as G protein-coupled receptor 120, is a long-chain fatty acid receptor highly expressed in adipocytes, endothelial cells, and macrophages. Activation of FFAR4 helps maintain metabolic homeostasis by regulating adipogenesis, insulin sensitivity, and inflammation. Furthermore, dysfunction of FFAR4 is associated with insulin resistance, obesity, and eccentric remodeling in both humans and mice, making FFAR4 an attractive therapeutic target for treating or preventing metabolic diseases. While much of the previous literature on FFAR4 has focused on its role in obesity and diabetes, recent studies have demonstrated that FFAR4 may also play an important role in the development of atherosclerosis and CVD. Most notably, FFAR4 activation reduces monocyte-endothelial cell interaction, enhances cholesterol efflux from macrophages, reduces lesion size in atherogenic mouse models, and stimulates oxylipin production in myocytes that functions in a feed-forward cardioprotective mechanism. This review will focus on the role of FFAR4 in metabolic diseases and highlights an underappreciated role of FFAR4 in the development of atherosclerosis and CVD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.