Cardiac arrest & resuscitation
Targeting branched-chain amino acid (BCAA)/PPAR-γ axis with pioglitazone reverses insulin resistance and mitigates post-cardiac arrest injury
Authors' conclusion
Dysregulated BCAA metabolism triggers IR via PPAR-γ suppression after CA, exacerbating ischemic brain injury.
Study context
- Population
- Cardiac arrest (CA) patients (retrospective cohort and prospective case-control), rat CA model and HT22 cell model121 CA patients retrospective cohort
- Participants
- 25 vs 21
- Comparison
- Pioglitazone after CA; CA patients vs controls
- CAn = 25
- Controlsn = 21reference
- Outcome
- Post-CA insulin resistance, BCAA/PPAR-γ pathway, survival and neurological function with pioglitazone (rat CA model)
Methodological detailsretrospective cohort, prospective case-control, rat CA model, HT22 cell oxygen-glucose deprivation/reperfusion model
- Retrospective cohort
- Prospective case-control
- Rat CA model
- HT22 cell oxygen-glucose deprivation/reperfusion model
Main finding
As reported in the abstract
Pioglitazone improved post-CA survival (P < 0.05)
40%
Pioglitazone improved Neurological Deficit Score (P < 0.001)
66.94 vs. 53.78
Original publication
Targeting BCAA/PPAR-γ axis with pioglitazone reverses insulin resistance and mitigates post-cardiac arrest injury. Resuscitation. Published 20 August 2026. doi:10.
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