What does this research mean for the field?

Interleukin-11 attenuates cardiac fibrosis following myocardial infarction through the activation of STAT3. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

January 26, 2010CirculationOpen Access

Therapeutic Activation of Signal Transducer and Activator of Transcription 3 by Interleukin-11 Ameliorates Cardiac Fibrosis After Myocardial Infarction

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Why the study?

Does Interleukin-11 ameliorate cardiac fibrosis after myocardial infarction?

Population

Post-myocardial infarction models

Design

Preclinical

Authors

MOMasanori ObanaHeart Failure & Transplant MMMakiko MaedaHeart Failure & Transplant KTKoji TakedaNewYork–Presbyterian Hospital

Discussion

Member takes

Implication

IL-11/STAT3 signaling merits testing in human post-MI trials; leaves open efficacy and safety in patients.

Structured PICO

Does Interleukin-11 ameliorate cardiac fibrosis after myocardial infarction?

Population

Post-myocardial infarction models

Intervention

Interleukin-11 (IL-11)

Outcome

Cardiac fibrosissurrogate

Activation of the IL-11/glycoprotein 130/STAT3 axis may serve as a novel therapeutic strategy to reduce cardiac fibrosis following myocardial infarction.

Cite This Study

Obana et al. (2010) studied this question.

synapsesocial.com/papers/69bc7d73642c8354f461c81d https://doi.org/10.1161/circulationaha.109.893677

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Therapeutic Activation of Signal Transducer and Activator of Transcription 3 by Interleukin-11 Ameliorates Cardiac Fibrosis After Myocardial Infarction

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Therapeutic Activation of Signal Transducer and Activator of Transcription 3 by Interleukin-11 Ameliorates Cardiac Fibrosis After Myocardial Infarction

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider