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Abstract
Sulforaphane (SFN) preserves mitochondrial-endoplasmic reticulum contact sites in cardiomyoblasts exposed to cobalt chloride-induced chemical hypoxia.
- Disruption of mitochondrial-endoplasmic reticulum contact sites negatively impacts cardiomyocyte function.
- SFN is investigated for its potential to enhance communication between these organelles.
- In rat cardiomyoblasts treated with SFN before exposure to cobalt chloride, mitochondrial-ER associations were maintained.
- The formation of autophagolysosomes was facilitated by preserved MERCS functionality.
- Autophagy may serve as the protective mechanism by which SFN supports cardiomyoblasts under chemical hypoxia.
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