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September 20, 2018Chinese Medical JournalOpen Access

Genetic overexpression of ATF3 in cardiac fibroblasts improved heart function after myocardial infarction, increasing cardiac ejection fraction to 41.0% compared to 30.5% in control mice.

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Why the study?

Does genetic overexpression of ATF3 specifically in cardiac fibroblasts improve cardiac function and reduce scar area in mice after myocardial infarction?

Population

35 male mice, 10-12 weeks old, subjected to myocardial infarction or sham operation.

Comparison

Genetic overexpression of Activating… vs Control mice without cardiac fibroblast-specific…

Design

Preclinical, Images analyzed by a person blinded to treatment.

Follow-up

28 days

Key result

Genetic overexpression of ATF3 in cardiac fibroblasts improved heart function after myocardial infarction, increasing cardiac ejection fraction to 41.0% compared to 30.5% in control mice.

Authors

YLYulin LiHuashan HospitalWHWenjing HaoInsermBCBo-Ya ChenBeijing Anzhen Hospital

Discussion

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Member takes

Overview

Should not change post-MI care; hypothesis-generating for fibroblast-targeted ATF3 therapy in humans.

Structured PICO

Does genetic overexpression of ATF3 specifically in cardiac fibroblasts improve cardiac function and reduce scar area in mice after myocardial infarction?

P
Population
35 male mice (15 C57BL/6 wild-type, 20 ATF3TGfl/flCol1a2-Cre+/-), 10-12 weeks old, subjected to myocardial infarction or sham operation.
I
Intervention
Genetic overexpression of Activating Transcription Factor 3 (ATF3) specifically in cardiac fibroblasts (ATF3TGfl/flCol1a2-Cre+).
C
Comparator
Control mice without cardiac fibroblast-specific ATF3 overexpression (ATF3TGfl/flCol1a2-Cre-).
O
Outcome
Cardiac function (ejection fraction and fractional shortening) measured by ultrasound and left ventricular remodeling (myocardial fibrosis area) measured by Masson staining at 28 days post-MI.surrogate

Main Result

Absolute Event Rate: 41% vs 30.5%

p-value: p=0.001

Cardiac fibroblast-specific overexpression of ATF3 promotes myocardial repair and improves cardiac function after myocardial infarction in a mouse model.

Cite This Study

Li et al. (2018) studied Myocardial infarction (n=35). Cardiac fibroblast-specific ATF3 overexpression vs. Without cardiac fibroblast-specific ATF3 overexpression was evaluated on Cardiac ejection fraction (p=0.001). Genetic overexpression of ATF3 in cardiac fibroblasts improved heart function after myocardial infarction, increasing cardiac ejection fraction to 41.0% compared to 30.5% in control mice.

synapsesocial.com/papers/6a1c2cd6ea84844e355f8c8fhttps://doi.org/10.4103/0366-6999.241794
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Induction of activating transcription factor 3 limits survival following infarct-induced heart failure in mice2015 · 28 citations
  2. 2ATF3 expression in cardiomyocytes and myofibroblasts following transverse aortic constriction displays distinct phenotypes2020 · 21 citations
  3. 3Cardiac Fibroblast–Specific Activating Transcription Factor 3 Protects Against Heart Failure by Suppressing MAP2K3-p38 Signaling2017 · 173 citations
  4. 4ATF3 is required for the prevention of cardiomyopathy via the regulation of mitochondrial oxidative stress2024
  5. 5Fast but not furious: neonatal cardiac fibroblasts as promoters of regeneration after myocardial infarction2024 · 1 citations