ReviewFrontiers in pharmacology2021
Mechanistic Insight into PPARγ and Tregs in Atherosclerotic Immune Inflammation.
Review in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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.
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Who cites it
22 citing papers in PubMed, 48 citations in OpenAlex.
- Bioinformatics identification of candidate biomarkers associated with T cell proliferation in atherosclerosis via WGCNA and machine learning.Journal of cardiothoracic surgery · 2026Article
- Hugan Tablets Alleviate Alcoholic Liver Injury by Modulating Hepatic Glutathione Metabolism and PPARγ/NRF2/GPX4-Related Antioxidant Defense.Pharmaceuticals (Basel, Switzerland) · 2026Article
- IL-17A deficiency in HLA-DR3 transgenic mice enriches beneficial Prevotella species in gut to promote Tregs and reduce CNS autoimmunity.Microbiome · 2026Article
- The GPR124‑Wnt‑PPARγ regulatory axis: Molecular mechanisms and therapeutic implications in chronic inflammatory diseases (Review).International journal of molecular medicine · 2026Review
- Jiangzhi ruanmai recipe alleviates atherosclerosis in ApoEFrontiers in cardiovascular medicine · 2026Article
- Relationship Between Carotid Intraplaque Neovascularization and Immune-Inflammatory Biomarkers with Coronary Stenosis.Reviews in cardiovascular medicine · 2025Article
- Immunometabolism and male reproductive function: linking inflammation, oxidative stress, and declining fertility.Frontiers in immunology · 2025Review
- Key Players in the Complex Pathophysiology of Obesity: A Cross-Talk Between the Obesogenic Genes and Unraveling the Metabolic Pathway of Action of Capsaicin and Orange Peel.Applied biochemistry and biotechnology · 2025Review
- Revisiting Tregs in cancer and beyond: immunological control and therapeutic potential.Frontiers in immunology · 2025Review
- PDCD4 promotes inflammation/fibrosis by activating the PPAR‑γ/NF‑κB pathway in mouse atrial myocytes.Molecular medicine reports · 2024Article
- Exploring the underlying molecular mechanisms of acute myocardial infarction after SARS-CoV-2 infection.American heart journal plus : cardiology research and practice · 2024Article
- Nobiletin alleviates atherosclerosis by inhibiting lipid uptake via the PPARG/CD36 pathway.Lipids in health and disease · 2024Article
- High plasma concentrations of vanin-1 in patients with coronary artery disease.Heart and vessels · 2024Article
- Editorial: New insights of immune cells in cardiovascular and metabolic disorders.Frontiers in immunology · 2023Article
- PPARγ (Peroxisome Proliferator-Activated Receptor γ) Deacetylation Suppresses Aging-Associated Atherosclerosis and Hypercholesterolemia.Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Potential intervention target of atherosclerosis: Ferroptosis (Review).Molecular medicine reports · 2022Review
- The Role of Transcription Factor PPAR-γ in the Pathogenesis of Psoriasis, Skin Cells, and Immune Cells.International journal of molecular sciences · 2022Review
- Metabolic profiles of regulatory T cells and their adaptations to the tumor microenvironment: implications for antitumor immunity.Journal of hematology & oncology · 2022Review
- Inhibition of VRK1 suppresses proliferation and migration of vascular smooth muscle cells and intima hyperplasia after injury via mTORC1/β-catenin axis.BMB reports · 2022Article
- Modified Lipoproteins Induce Arterial Wall Inflammation During Atherogenesis.Frontiers in cardiovascular medicine · 2022Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis (AS) is the main pathological cause of acute cardiovascular and cerebrovascular diseases, such as acute myocardial infarction and cerebral apoplexy. As an immune-mediated inflammatory disease, the pathogenesis of AS involves endothelial cell dysfunction, lipid accumulation, foam cell formation, vascular smooth muscle cell (VSMC) migration, and inflammatory factor infiltration. The nuclear receptor peroxisome proliferator-activated receptor gamma (PPARγ) plays an important role in lipid metabolism, inflammation, and apoptosis by antagonizing the Wnt/β-catenin pathway and regulating cholesterol efflux and inflammatory factors. Importantly, PPARγ-dependant fatty acid uptake is critical for metabolic programming. Activated PPARγ can exert an anti-atherosclerotic effect by inhibiting the expression of various inflammatory factors, improving endothelial cell function, and restraining the proliferation and migration of VSMCs. Regulatory T cells (Tregs) are the only subset of T lymphocytes that have a completely negative regulatory effect on the autoimmune response. They play a critical role in suppressing excessive immune responses and inflammatory reactions and widely affect AS-associated foam cell formation, plaque rupture, and other processes. Recent studies have shown that PPARγ activation promotes the recruitment of Tregs to reduce inflammation, thereby exerting its anti-atherosclerotic effect. In this review, we provide an overview of the anti-AS roles of PPARγ and Tregs by discussing their pathological mechanisms from the perspective of AS and immune-mediated inflammation, with a focus on basic research and clinical trials of their efficacies alone or in combination in inhibiting atherosclerotic inflammation. Additionally, we explore new ideas for AS treatment and plaque stabilization and establish a foundation for the development of natural PPARγ agonists with Treg recruitment capability.
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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.