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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.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability
All data generated or analyzed during this study are included in this published article.