Abstract
Context: Mammalian STE20-like protein kinases 1 (MST1) has been found to be associated with cardiomyocyte damage following acute myocardial infarction.Aim: The aim of our study is to explore the influence of MST1 in inflammation response following myocardial infarction.Methods: Cardiomyocyte cell line was used in vitro with hypoxia treatment to establish myocardial infarction model. ELISA, qPCR, Western blots, and siRNA technology were used to analyze the role of MST1 in inflammation response following myocardial infarction.Results: The transcription and expression of MST1 was significantly elevated following myocardial infarction. Loss of MST1 attenuated the levels of inflammation response and thus contributed to the survival of cardiomyocyte in vitro. Mechanistically, MST1 deletion reversed the activity of heme oxygenase-1 (HO-1) and thus reduced hypoxia-mediated cardiomyocyte death.Conclusions: Altogether, in this study, we found that MST1-Hippo pathway is activated in myocardial infarction and contributes to the inflammation response in cardiomyocytes through inhibiting the HO-1 signaling pathway. This finding would provide a potential target to reverse cardiomyocyte viability and reduce inflammation response in myocardial infarction.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
