ABHD11-Mediated mtDNA Transcription Restored Mitochondrial Function to Attenuate Cardiomyocyte Ferroptosis After Myocardial Infarction
Authors' conclusion
This study revealed that ABHD11-mediated mitochondrial DNA transcription attenuated cardiomyocyte ferroptosis after MI by orchestrating a mitochondrial-nuclear crosstalk
Study context
- Population
- Murine post-MI hearts and human myocardial infarction (MI) hearts
Methodological detailsmurine MI models, loss- and gain-of-function approaches
- Murine MI models
- Loss- and gain-of-function approaches
Main finding
As reported in the abstract
- Cardiac ferroptosis peaked at day 7 after MI, enriched in peri-infarct cardiomyocytes
- Mitochondrial dysfunction was a key driver of cardiomyocyte ferroptosis after MI; ABHD11 identified as potential regulator
- ABHD11 expression reduced in mouse and human MI hearts; transcription repressed by DNMT1-mediated promoter hypermethylation
- Cardiac-specific ABHD11 overexpression alleviated cardiomyocyte ferroptosis and improved cardiac function after MI
- Loss of ABHD11 in adult mice exacerbated pathological cardiac remodeling and HF
- ABHD11 acted as mtDNA transcription coactivator by enhancing TEFM-POLRMT interaction, independent of canonical enzymatic activities, restoring mitochondrial function and reducing lipid peroxidation and 4-hydroxynonenal
- Reduced 4-hydroxynonenal stabilized YY1, which regulated ferroptosis-driving genes, inhibiting ferroptosis and promoting cardiac recovery
Original publication
ABHD11-Mediated mtDNA Transcription Restored Mitochondrial Function to Attenuate Cardiomyocyte Ferroptosis After Myocardial Infarction. Circulation. Published 11 August 2026. doi:10.
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