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July 8, 2016Journal of Molecular and Cellular CardiologyOpen Access

Cardiomyocyte hypertrophy and interstitial fibrosis were augmented in cardio-Nox2TG compared to WT after MI, whereas endo-Nox2TG mice showed no significant difference compared to WT.

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Population

Transgenic mouse models and matched wild-type littermates subjected to myocardial infarction induced by…

Comparison

Targeted Nox2 expression in cardiomyocytes or… vs Matched wild-type littermates (WT)

Design

Preclinical

Follow-up

up to 4 weeks

Authors

ASAlexander SirkerCMColin E. MurdochAPAndrea Protti

Discussion

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Overview

Suggests cardiomyocyte Nox2 as remodeling target post-MI; leaves open human translation.

Structured PICO

P
Population
Transgenic mouse models (cardio-Nox2TG and endo-Nox2TG) and matched wild-type littermates (WT) subjected to myocardial infarction induced by permanent left coronary artery ligation
I
Intervention
Targeted Nox2 expression in cardiomyocytes (cardio-Nox2TG) or endothelial cells (endo-Nox2TG)
C
Comparator
Matched wild-type littermates (WT)
O
Outcome
Response to MI including initial infarct size, cardiac dysfunction, cardiomyocyte hypertrophy, interstitial fibrosis, and post-MI survivalsurrogate

Cardiomyocyte-specific, rather than endothelial cell-specific, Nox2 expression plays a more important role in adverse cardiac remodeling after myocardial infarction.

Cite This Study

Sirker et al. (2016) studied this question.

synapsesocial.com/papers/6a21436ca2a97f3a085ae040https://doi.org/10.1016/j.yjmcc.2016.07.003
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