Integrating network toxicology and transcriptomics reveals the potential targets of chlorfenapyr-induced myocardial injury - PubMed
3 hours ago
- #Chlorfenapyr
- #Transcriptomics
- #Myocardial Injury
- Chlorfenapyr is a novel insecticide known to induce acute myocardial injury and cardiotoxicity.
- The study used network toxicology and transcriptomic profiling to investigate potential targets of chlorfenapyr-induced myocardial injury.
- Exposed rats showed elevated body temperatures, abnormal cardiac function, myocardial injury, and increased levels of cardiac biomarkers.
- Five key targets (KCNA5, ICAM1, KCNJ6, PTGS2, and PIM1) were identified, linked to pathways involving inflammation, apoptosis, ion homeostasis, TNF, and NF-kappa B signaling.
- Molecular docking confirmed stable binding interactions, and chlorfenapyr reduced cell viability, increased apoptosis, and induced mitochondrial dysfunction in H9c2 cells.
- The differential expression of Icam1, Ptgs2, and Kcna5 was validated in both H9c2 cells and rat heart tissue, aligning with transcriptomic data.
- The study concludes that these targets and mechanisms may play a role in chlorfenapyr-induced myocardial injury, warranting further investigation.