Arrhythmias & electrophysiology
SLC31A1 loss depletes mitochondrial copper and promotes cardiac fibrosis
Authors' conclusion
A novel epigenetic mechanism was demonstrated through which copper deficiency increases mitochondrial copper depletion and impairs CF.
Study context
- Population
- Mouse models of cardiac fibrosis (isoprenaline/angiotensin II); human heart tissue from AF patients
Main finding
As reported in the abstract
- Lower copper concentrations with SLC31A1 down-regulation and mitochondrial copper depletion in cardiac fibrosis (CF)
- Fibroblast-specific SLC31A1 deficiency enhances mitochondrial copper depletion, augments glycolysis, promotes fibroblast proliferation and triggers CF
- Increased MeCP2-recognized methylation of SLC31A1 promoter CpG islands restrains its transcription; MeCP2 knockdown rescued SLC31A1 expression
- MeCP2 up-regulation associated with elevated m6A mRNA levels; YTHDF1 recognizes MeCP2 mRNA and induces its translation
- AF patients' heart tissue: reduced copper and SLC31A1, elevated YTHDF1 and MeCP2, associated with mitochondrial copper depletion, enhanced glycolysis and CF
Original publication
SLC31A1 loss depletes mitochondrial copper and promotes cardiac fibrosis. Eur Heart J. Published 6 March 2025. doi:10.
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