ArticleScientific reports2024
Unveiling potential drug targets for hyperparathyroidism through genetic insights via Mendelian randomization and colocalization analyses.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 12 citations in OpenAlex.
- Identification of DHX58 as a potential therapeutic target for ovarian cancer through multi-omics Mendelian randomization and transcriptomic data analysis.Journal of ovarian research · 2026Article
- PSMA4 as a Druggable Target in Hidradenitis Suppurativa: Evidence From Mendelian Randomization and Single-Cell Transcriptomics.Mediators of inflammation · 2026Article
- DNA methylation and bronchiectasis: a Mendelian randomization analysis to investigate causal link and therapeutic target.Epigenetics · 2025Article
- Identification of potential bladder cancer drug targets through Mendelian randomization and molecular docking.Discover oncology · 2025Article
- Regulatory polymorphisms ofJournal for immunotherapy of cancer · 2025Article
- Identifying causal genes for prostatitis through drug-targeted Mendelian randomization.Scientific reports · 2025Article
- A genome-wide association study of European advanced cancer patients treated with opioids identifies regulatory variants on chromosome 20 associated with pain intensity.European journal of pain (London, England) · 2025Article
- Deciphering the role of SEMA4A/MAPK signaling in sepsis: insights from Mendelian randomization, transcriptomic, single-cell sequencing analyses, and vitro experiments.Frontiers in cellular and infection microbiology · 2025Article
- Precision stratified treatment of primary hyperparathyroidism based on multilevel emerging biomarkers.Frontiers in endocrinology · 2025Review
- Unveiling therapeutic targets for spinal stenosis from genetic insights: a Mendelian randomization analysis.Scientific reports · 2024Article
- Multi-omics Mendelian randomization integrating GWAS, eQTL and pQTL data revealed GSTM4 as a potential drug target for migraine.The journal of headache and pain · 2024Article
- Therapeutic targets for lung cancer: genome-wide Mendelian randomization and colocalization analyses.Frontiers in pharmacology · 2024Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Hyperparathyroidism (HPT) manifests as a complex condition with a substantial disease burden. While advances have been made in surgical interventions and non-surgical pharmacotherapy for the management of hyperparathyroidism, radical options to halt underlying disease progression remain lacking. Identifying putative genetic drivers and exploring novel drug targets that can impede HPT progression remain critical unmet needs. A Mendelian randomization (MR) analysis was performed to uncover putative therapeutic targets implicated in hyperparathyroidism pathology. Cis-expression quantitative trait loci (cis-eQTL) data serving as genetic instrumental variables were obtained from the eQTLGen Consortium and Genotype-Tissue Expression (GTEx) portal. Hyperparathyroidism summary statistics for single nucleotide polymorphism (SNP) associations were sourced from the FinnGen study (5590 cases; 361,988 controls). Colocalization analysis was performed to determine the probability of shared causal variants underlying SNP-hyperparathyroidism and SNP-eQTL links. Five drug targets (CMKLR1, FSTL1, IGSF11, PIK3C3 and SLC40A1) showed significant causation with hyperparathyroidism in both eQTLGen and GTEx cohorts by MR analysis. Specifically, phosphatidylinositol 3-kinase catalytic subunit type 3 (PIK3C3) and solute carrier family 40 member 1 (SLC40A1) showed strong evidence of colocalization with HPT. Multivariable MR and Phenome-Wide Association Study analyses indicated these two targets were not associated with other traits. Additionally, drug prediction analysis implies the potential of these two targets for future clinical applications. This study identifies PIK3C3 and SLC40A1 as potential genetically proxied druggable genes and promising therapeutic targets for hyperparathyroidism. Targeting PIK3C3 and SLC40A1 may offer effective novel pharmacotherapies for impeding hyperparathyroidism progression and reducing disease risk. These findings provide preliminary genetic insight into underlying drivers amenable to therapeutic manipulation, though further investigation is imperative to validate translational potential from preclinical models through clinical applications.
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