Reproductive toxicology (Elmsford, N.Y.) · 2025
IGF1R as a protective target in antidiabetic drug-mediated prevention of erectile dysfunction: Insights from genetics.
СтатьяМетаанализПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Li Yuqi, Wang Juan, Zhou Tao, Liu Zhiyu, Meng Chunyang, Deng Qingfu
Аннотация
BACKGROUND: In recent years, antidiabetic drugs have been increasingly repurposed for conditions beyond diabetes. However, their effects on erectile dysfunction (ED) remain inadequately understood. This study utilizes Mendelian randomization (MR) analysis to investigate the potential impact of antidiabetic drug targets on the risk of ED.
METHOD: We retrieved target gene information for eight classes of antidiabetic drugs from the DrugBank and GeneCards databases and subsequently identified instrumental variables for the corresponding genes using data from the eQTLGen consortium. Following data integration, we conducted MR, meta-analysis, and summary-data-based mendelian randomization (SMR) to systematically investigate the potential causal relationship between antidiabetic drug target genes and ED. Furthermore, we performed sensitivity analyses to assess the robustness and reliability of the observed associations.
RESULT: This study investigated the potential association between 24 antidiabetic drug target genes and ED, identifying 11 positive target genes and included in subsequent analyses. Using MR, meta-analysis, and summary-data-based MR, we observed a significant negative correlation between IGF1R and ED (OR 0.907, 95 % CI 0.859-0.959, P < 0.001). These findings suggest that IGF1R may exert a protective effect against ED, offering novel theoretical support for the potential repurposing of antidiabetic drugs in ED treatment.
CONCLUSION: Our findings indicate that elevated expression of IGF1R may be associated with a reduced risk of erectile dysfunction (ED). This observation implies that the rational application of insulin and its analogs could confer potential preventive benefits against ED, offering novel theoretical insights for the development of targeted therapeutic strategies.
METHOD: We retrieved target gene information for eight classes of antidiabetic drugs from the DrugBank and GeneCards databases and subsequently identified instrumental variables for the corresponding genes using data from the eQTLGen consortium. Following data integration, we conducted MR, meta-analysis, and summary-data-based mendelian randomization (SMR) to systematically investigate the potential causal relationship between antidiabetic drug target genes and ED. Furthermore, we performed sensitivity analyses to assess the robustness and reliability of the observed associations.
RESULT: This study investigated the potential association between 24 antidiabetic drug target genes and ED, identifying 11 positive target genes and included in subsequent analyses. Using MR, meta-analysis, and summary-data-based MR, we observed a significant negative correlation between IGF1R and ED (OR 0.907, 95 % CI 0.859-0.959, P < 0.001). These findings suggest that IGF1R may exert a protective effect against ED, offering novel theoretical support for the potential repurposing of antidiabetic drugs in ED treatment.
CONCLUSION: Our findings indicate that elevated expression of IGF1R may be associated with a reduced risk of erectile dysfunction (ED). This observation implies that the rational application of insulin and its analogs could confer potential preventive benefits against ED, offering novel theoretical insights for the development of targeted therapeutic strategies.