Key result
Optic atrophy factor-1 haploinsufficiency drives sympathetic denervation and arrhythmias via disrupted mitochondrial dynamics.
OPA1 deficiency disrupts mitochondrial dynamics and neurotrophic signaling, driving sympathetic neurodegeneration and arrhythmias in dominant optic atrophy.
Peripheral sympathetic neurodegeneration drives cardiac dysfunction in dominant optic atrophy, revealing a critical neuro-cardiac link. Optic atrophy factor-1 haploinsufficiency disrupts mitochondrial dynamics and neurotrophic signaling, causing targeted sympathetic denervation and arrhythmias. Restoring nerve growth factor transport and mitochondrial health in sympathetic neurons represents a promising therapeutic avenue for cardiac autonomic disorders. Future research must unravel mechanisms of neurocardiac crosstalk to develop precise interventions against neurogenic cardiac disease progression.
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Ronfini et al. (2026) studied Dominant optic atrophy. Optic atrophy factor-1 haploinsufficiency was evaluated on Sympathetic denervation and arrhythmias. Optic atrophy factor-1 haploinsufficiency disrupts mitochondrial dynamics and neurotrophic signaling, causing targeted sympathetic denervation and arrhythmias.
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