Sulforaphane protects cardiomyoblasts against chemical hypoxia by increasing mitochondrial-ER communication and autophagy.

Disruption of the contact sites between mitochondria and the endoplasmic reticulum (MERCSs) adversely affects cardiomyocyte function, necessitating interventions to preserve these connections and maintain the cellular homeostasis. Currently, the nutraceutical sulforaphane (SFN) has emerged as a promising candidate for enhancing MERCSs communication and offering protection in various contexts. In this study, we investigated whether SFN preserves MERCSs functionality in cardiomyoblasts subjected to cobalt chloride (CoCl2)-induced chemical hypoxia. We explored cellular events, including oxidative stress, endoplasmic reticulum stress (ERS), and autophagy, which are regulated by MERCSs. Our findings confirmed that in rat cardiomyoblasts H9c2 pretreated with SFN and exposed to CoCl2, mitochondrial-ER associations were maintained, facilitating the formation of autophagolysosomes. This suggest that autophagy is a mechanism through which SFN protects cardiomyoblasts under chemical hypoxia. This study underscores the significance of MERCSs as functional platforms for maintaining cellular homeostasis and highlights their potential as strategic targets for mitigating the harmful effects of hypoxia in cardiomyoblasts.