ArticleJournal of advanced research2025
Genetic associations of metabolic factors and therapeutic drug targets with polycystic ovary syndrome.
Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed.
- Effects of combined oral contraceptives and metformin on paraoxonase 1 lactonase activity and status in patients with polycystic ovary syndrome and insulin resistance.Frontiers in endocrinology · 2025Trial
- The Role and Mechanism of Incretins in Gynaecologic Diseases.Endocrinology, diabetes & metabolism · 2026Review
- Alnustone ameliorates obesity and polycystic ovary syndrome by remodeling adipose metabolism via AMPK signaling.Science China. Life sciences · 2026Article
- Exosomal miR-199a-3p derived from follicular fluid modulates the immune microenvironment in polycystic ovary syndrome by regulating macrophage polarization.Journal of ovarian research · 2026Article
- Long-chain fatty acids as functional modulators in PCOS: metabolic crosstalk, signaling pathways, and therapeutic implications.Frontiers in nutrition · 2026Review
- Remission of polycystic ovary syndrome based on the recovery of ovarian morphology identified by three-dimensional ultrasonography: a retrospective study.Frontiers in endocrinology · 2026Article
- Triglycerides and ovarian response in diminished ovarian reserve: a two-sample mendelian randomization and clinical mediation study.Frontiers in endocrinology · 2026Article
- Integrative multi-omics analysis of druggable genes for therapeutic target identification in polycystic ovary syndrome.Journal of ovarian research · 2025Article
- Cholesterol metabolism and cancer: Molecular mechanisms, immune regulation and an epidemiological perspective (Review).International journal of molecular medicine · 2025Review
- Integrated transcriptomic and co-expression network analysis identifies immune-metabolic biomarkers of polycystic ovary syndrome in granulosa cells.Journal of ovarian research · 2025Article
- The Effects ofFood science & nutrition · 2025Article
- Association between delayed methotrexate metabolism, coagulation function, and adverse reactions in patients with acute lymphoblastic leukemia receiving high-dose methotrexate treatment.American journal of translational research · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionPolycystic ovary syndrome (PCOS) is frequently accompanied with metabolic dysfunctions, yet the causal relationships between metabolic factors and PCOS remain to be conclusively established and etiology-based therapies are lacking.
objectivesTo comprehensively identify the metabolic causal factors and potential drug targets for PCOS.
methodsThis genetic association study was conducted using bidirectional two-sample Mendelian Randomization (MR), multivariable MR (MVMR) and drug-target MR. Considering metabolic sexual dimorphism, female-specific genome-wide association studies (GWASs) for metabolic factors were obtained. To ensure the robustness of the findings, an additional independent PCOS GWAS dataset was utilized for replication.
resultsThe PCOS cohort included 10,074 PCOS cases (mean age 28 to 45 years) and 103,164 controls (mean age 27 to 60 years) of European ancestry. All participants were female. Employing two-sample MR analysis, we found that genetically proxied body mass index (BMI) (OR = 3.40 [95 % CI, 2.65-4.36]), triglyceride (TG) (OR = 1.54 [95 % CI, 1.17-2.04]), low-density lipoprotein cholesterol (LDL-c) (OR = 1.37 [95 % CI, 1.07-1.76]), and type 2 diabetes (T2D) (OR = 1.24 [95 % CI, 1.09-1.41]) were significantly associated with an increased risk of PCOS, whereas genetically predicted high-density lipoprotein cholesterol (HDL-c) (OR = 0.61 [95 % CI, 0.47-0.80]) decreased the odds of PCOS. Stepwise MVMR established a hierarchy of interactions among these metabolic factors, identifying BMI and HDL-c as the most prominent causal factors. Notably, drug-target MR analysis identified incretin-based therapeutics, PCSK9 inhibitors, LPL gene therapy, sulfonylureas, and thiazolidinediones as potential therapeutics for PCOS. All these findings were validated in an independent dataset.
conclusionThis study offered insights into the roles of obesity, diabetes, and dyslipidemia in PCOS etiology and therapeutics, underscoring the necessity for managing metabolic health in women and paving the way for tailored therapeutic strategies for PCOS based on its metabolic underpinnings.
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.