Knockdown of OLFM4 protects cardiomyocytes from sepsis by inhibiting apoptosis and inflammatory responses

• Hailu Chen ^[1] ; Shuna Liu ^[1] ; Guihua Fang ^[1]
  1. [1] Department of Infectious Diseases and Tropical Diseases, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, China
• Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 52, Nº. 5, 2024, págs. 15-20
• Idioma: inglés
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• Resumen

  • Sepsis is a systemic inflammatory response that can result in cardiac insufficiency or heart failure known as septic myocardial injury. A previous study identified OLFM4 as an important gene in sepsis through bioinformatics analysis. However, there is limited research on the regulatory functions of OLFM4 in sepsis-triggered myocardial injury, and the related molecular mechanisms remain unclear. In this study, the protein expression of OLFM4 was found to be significantly elevated in LPS-stimulated H9C2 cells, and its suppression enhanced cell proliferation and reduced cell apoptosis in LPS-triggered H9C2 cells. The inflammatory factors TNF-α, IL-6, and IL-1β were increased after LPS treatment, and these effects were mitigated after silencing OLFM4. Moreover, it was confirmed that inhibition of OLFM4 attenuated the NF-κB signaling pathway. In conclusion, the knockdown of OLFM4 protected cardiomyocytes from sepsis by inhibiting apoptosis and inflammatory responses via the NF-κB pathway. These findings provide important insights into the regulatory functions of OLFM4 in the progression of septic myocardial injury.