USP18 mediates high glucose-induced cardiomyocyte injury by regulating the JAK/STAT signaling pathway through stabilizing FOXC2 expression.

Puntos clave

• This research aims to explore how USP18 influences cardiac injury under high glucose conditions by regulating FOXC2 expression.
• Investigated the role of USP18 in cardiomyocytes under high glucose exposure.
• Analyzed ubiquitination levels of FOXC2 influenced by USP18.
• Examined the activation of the JAK/STAT signaling pathway in response to changes in FOXC2 expression.
• FOXC2 expression was stabilized by USP18, reducing myocardial injury under high glucose.
• Inhibition of ubiquitination led to increased FOXC2 levels, suggesting a protective role against cardiac damage.
• Activation of the JAK/STAT pathway correlated with changes in FOXC2 expression and myocardial health.

Resumen