What is the clinical evidence from this study?

Study design: Other. Population: Myocardial ischemia/reperfusion injury (n=62). Intervention: WY-14643 vs. DMSO solvent (untreated controls). Primary outcome: Size of myocardial infarction (% of area at risk) (p=<0.05).

What does this research mean for the field?

Upregulation of PPAR-alpha target metabolic genes involved in fatty acid oxidation, along with activation of the PI3K/Akt/eNOS pathway, enhances myocardial resistance to ischemia/reperfusion injury in the rat heart. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

November 12, 2013Physiological ResearchOpen Access

Upregulation of Genes Involved in Cardiac Metabolism Enhances Myocardial Resistance to Ischemia/Reperfusion in the Rat Heart

Q: What are the key findings of this study?

Pretreatment with the PPAR-alpha agonist WY-14643 significantly reduced myocardial infarct size from 34% to 18% compared to controls in rat hearts exposed to ischemia/reperfusion.

Q: What does this research mean for the field?

Upregulation of PPAR-alpha target metabolic genes involved in fatty acid oxidation, along with activation of the PI3K/Akt/eNOS pathway, enhances myocardial resistance to ischemia/reperfusion injury in the rat heart. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

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Key result

Pretreatment with the PPAR-alpha agonist WY-14643 significantly reduced myocardial infarct size from 34% to 18% compared to controls in rat hearts exposed to ischemia/reperfusion.

Why the study?

Does pretreatment with PPAR-alpha agonist WY-14643 reduce ischemia/reperfusion injury in a rat heart model?

Population

Rat heart model of ischemia/reperfusion injury

Design

Preclinical

Follow-up

2-h reperfusion

Authors

TRT RavíngerováSlovak Academy of Sciences SČSlávka ČarnickáSlovak Academy of Sciences VLV. LEDVÉNYIOVÁSlovak Academy of Sciences

Discussion

Member takes

Implication

May support metabolic cardioprotection strategies; leaves open translation from rat models to clinical ischemia/reperfusion injury.

Structured PICO

Does pretreatment with PPAR-alpha agonist WY-14643 reduce ischemia/reperfusion injury in a rat heart model?

Population

Rat heart model of ischemia/reperfusion (I/R) injury (isolated hearts exposed to 30-min global ischemia and 2-h reperfusion)

Intervention

Pretreatment with PPAR-alpha agonist WY-14643 (1 mg/kg, i.p.) 24 h prior to ischemia/reperfusion

Outcome

Post-ischemic stunning, arrhythmias, extent of lethal injury (infarct size), and apoptosis (caspase-3 expression)surrogate

Main Result

Absolute Event Rate: 18% vs 34%

p-value: p=<0.05

PPAR-alpha activation prior to ischemia/reperfusion in a rat model reduces myocardial injury, potentially via metabolic shifts toward fatty acid oxidation and activation of the PI3K/Akt/eNOS pathway.

Limitations

Cannot exclude that other proteins involved in the PI3K/Akt-dependent mitochondrial apoptotic pathway might also contribute to the observed cardioprotective effects

Cite This Study

Ravíngerová et al. (2013) studied Myocardial ischemia/reperfusion injury (n=62). WY-14643 vs. DMSO solvent (untreated controls) was evaluated on Size of myocardial infarction (% of area at risk) (p=<0.05). Pretreatment with the PPAR-alpha agonist WY-14643 significantly reduced myocardial infarct size from 34% to 18% compared to controls in rat hearts exposed to ischemia/reperfusion.

synapsesocial.com/papers/6a0a1e0900274e073d45d9ae https://doi.org/10.33549/physiolres.932597

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Upregulation of Genes Involved in Cardiac Metabolism Enhances Myocardial Resistance to Ischemia/Reperfusion in the Rat Heart

Discussion

Member takes

Implication

Structured PICO

Main Result

Limitations

Cite This Study

Upregulation of Genes Involved in Cardiac Metabolism Enhances Myocardial Resistance to Ischemia/Reperfusion in the Rat Heart

Discussion

Member takes

Implication

Structured PICO

Main Result

Limitations

Cite This Study

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Also Consider