Scpep1 inhibition attenuates myocardial infarction-induced dysfunction by improving mitochondrial bioenergetics
An erratum to this article was published (Eur Heart J, 3 Nov 2025 ↗)
Authors' conclusion
Scpep1 deficiency mitigates MI by improving Pex3-mediated mitochondrial fission and subsequent cardiomyocyte apoptosis.
Study context
- Population
- Mice with myocardial infarction (MI); plasma and heart tissue of patients with MI or ischaemic cardiomyopathy
- Comparison
- Scpep1 deficiency or cardiac-specific knock-down vs Scpep1 overexpression in mice with MI
Main finding
As reported in the abstract
- Circulating and cardiac Scpep1 up-regulated in mice with MI
- Genetic ablation or cardiac-specific knock-down of Scpep1 alleviated MI-induced cardiac dysfunction and damage
- Cardiac-specific Scpep1 overexpression aggravated these adverse effects
- Scpep1 impaired mitochondrial bioenergetics by binding Pex3 to promote its degradation, leading to mitochondrial fission and apoptosis
- Scpep1 expression in plasma and heart tissue of patients with MI or ischaemic cardiomyopathy in line with mouse models
- Pharmaceutical Scpep1 inhibition improved MI-induced cardiac dysfunction and damage via improved mitochondrial fragmentation and bioenergetics
Original publication
Scpep1 inhibition attenuates myocardial infarction-induced dysfunction by improving mitochondrial bioenergetics. Eur Heart J. Published 11 February 2025. doi:10.
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