October 21, 2003CirculationOpen Access

Opposing Effects Mediated by the Chemokine Receptor CXCR2 on Myocardial Ischemia-Reperfusion Injury

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Why the study?

Does CXCR2 knockout reduce myocardial ischemia-reperfusion injury in mice?

Structured PICO

Does CXCR2 knockout reduce myocardial ischemia-reperfusion injury in mice?

Population

CXCR2-/- mice and wild type mice undergoing myocardial ischemia-reperfusion in vivo, lethally irradiated wild type mice reconstituted with bone marrow, and isolated Langendorff heart preparations

Intervention

CXCR2 knockout (genetic deletion or bone marrow reconstitution)

Comparator

Wild type mice or wild type bone marrow reconstitution

Outcome

Infarct size and number of inflammatory cellssurrogate

CXCR2 exerts opposing effects during myocardial ischemia-reperfusion, where its role in recruiting damaging inflammatory cells outweighs its direct cardioprotective effects.

Authors

STSima T. TarzamiHoward University WMWenfeng MiaoTianjin University of Science and Technology KMKartik ManiHeart Rhythm Society

Discussion

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Implication

Should not alter clinical reperfusion strategies; leaves open selective CXCR2 targeting to balance inflammatory and cardioprotective effects.

Cite This Study

Tarzami et al. (2003) studied this question.

synapsesocial.com/papers/6a710a7587f9210571280853 https://doi.org/10.1161/01.cir.0000093192.72099.9a

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Implication

Should not alter clinical reperfusion strategies; leaves open selective CXCR2 targeting to balance inflammatory and cardioprotective effects.

Opposing Effects Mediated by the Chemokine Receptor CXCR2 on Myocardial Ischemia-Reperfusion Injury

Structured PICO

Discussion

Implication

Cite This Study

Opposing Effects Mediated by the Chemokine Receptor CXCR2 on Myocardial Ischemia-Reperfusion Injury

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider