ReviewBiomolecules2024
PPARγ Modulators in Lung Cancer: Molecular Mechanisms, Clinical Prospects, and Challenges.
Review in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 23 citations in OpenAlex.
- Pachymic acid exhibits synergistic antitumor efficacy with lenvatinib in hepatocellular carcinoma by targeting PPARγ to inhibit glycolysis.Medical oncology (Northwood, London, England) · 2026Article
- Multi-omics investigation of per- and polyfluoroalkyl substances in lung adenocarcinoma: comprehensive network toxicology, machine learning and molecular docking experiments.Molecular diversity · 2026Article
- T-Cell Exhaustion in the Tumor Microenvironment: Subcellular Dysfunction, Pan-Cancer Characteristics, and Therapeutic Interventions.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Genetic influence of PPAR-γ rs1801282 and MTRR rs162036 variants on non-small cell lung cancer risk in Egyptians.Discover oncology · 2026Article
- Article
- From concept to application: Exploring the evolution and potential of DUBTAC technology.Acta pharmaceutica Sinica. B · 2026Review
- Long-Chain Fatty Acids Inhibit Myeloid-Derived Suppressor Cells to Delay Tumor Progression.Current issues in molecular biology · 2026Article
- Article
- PPARγ: a key orchestrator of epidermal barrier, immune responses, and lipid metabolism in atopic dermatitis pathogenesis and therapy.Frontiers in allergy · 2026Review
- Pioglitazone-Based Combination Approaches for Non-Small-Cell Lung Cancer.Pharmaceutics · 2025Review
- Exploration of isolated actives from Coleus amboinicus leaves as anticancer agents: in vitro testing, network pharmacology studies, and molecular docking.Scientific reports · 2025Article
- Treatment of non-small cell lung cancer using chem-bioinformatics-driven engineering of exosomal cargo-vehicle for telmisartan and pioglitazone targeted-delivery.Scientific reports · 2025Article
- Ethanolic Extract ofPharmaceuticals (Basel, Switzerland) · 2025Article
- Chemical Composition and Anti-Lung Cancer Activities ofPharmaceuticals (Basel, Switzerland) · 2025Article
- Thiazolidinedione derivatives in cancer therapy: exploring novel mechanisms, therapeutic potentials, and future horizons in oncology.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Uncovering Novel Anti-Lung Cancer Compounds: Insights from Marine Sponge-Derived Agents: A Bibliometric Review.Iranian journal of medical sciences · 2025Review
- EGCG alleviates PM2.5-induced lung injury via activation of PPAR-γ to suppress inflammation and oxidative stress.Frontiers in pharmacology · 2025Article
- The role of PPARγ in cancer cachexia: friend or foe?Frontiers in endocrinology · 2025Review
- Multiple signaling pathways in the frontiers of lung cancer progression.Frontiers in immunology · 2025Review
- Detection of serum SNHG22 and its correlation with prognosis of non-small cell lung cancer.Journal of cardiothoracic surgery · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Lung cancer is one of the most lethal malignancies worldwide. Peroxisome proliferator-activated receptor gamma (PPARγ, NR1C3) is a ligand-activated transcriptional factor that governs the expression of genes involved in glucolipid metabolism, energy homeostasis, cell differentiation, and inflammation. Multiple studies have demonstrated that PPARγ activation exerts anti-tumor effects in lung cancer through regulation of lipid metabolism, induction of apoptosis, and cell cycle arrest, as well as inhibition of invasion and migration. Interestingly, PPARγ activation may have pro-tumor effects on cells of the tumor microenvironment, especially myeloid cells. Recent clinical data has substantiated the potential of PPARγ agonists as therapeutic agents for lung cancer. Additionally, PPARγ agonists also show synergistic effects with traditional chemotherapy and radiotherapy. However, the clinical application of PPARγ agonists remains limited due to the presence of adverse side effects. Thus, further research and clinical trials are necessary to comprehensively explore the actions of PPARγ in both tumor and stromal cells and to evaluate the in vivo toxicity. This review aims to consolidate the molecular mechanism of PPARγ modulators and to discuss their clinical prospects and challenges in tackling lung cancer.
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.