October 4, 2018Biomedicine & PharmacotherapyOpen Access

Overexpression of miR-142-3p improves mitochondrial function in cardiac hypertrophy

Q: What is the clinical evidence from this study?

Study design: Other. Population: Cardiac hypertrophy. Intervention: miR-142-3p overexpression vs. Pressure overload/AngII without miR-142-3p overexpression. Primary outcome: Cardiac hypertrophy and mitochondrial function.

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Key result

Overexpression of miR-142-3p mitigated cardiac hypertrophy and protected mitochondrial function in vitro and in vivo by directly inhibiting SH2B1 expression.

Why the study?

Does overexpression of miR-142-3p mitigate cardiac hypertrophy and improve mitochondrial function in preclinical models?

Population

Rat model of pressure overload myocardial hypertrophy induced by abdominal aorta ligation and cultured…

Comparison

Overexpression of miR-142-3p via miR-142-3p… vs Abdominal aorta ligation without miR-142-3p…

Design

Preclinical

Follow-up

4 weeks (in vivo)

Authors

BLBeilei LiuShanghai Jiao Tong University MCMian ChengTongji Hospital SHShan HuChina Automotive Engineering Research Institute

Discussion

Member takes

Implication

Hypothesis-generating for miR-142-3p in hypertrophy; leaves open human translation and trials.

Structured PICO

Does overexpression of miR-142-3p mitigate cardiac hypertrophy and improve mitochondrial function in preclinical models?

Population

Rat model of pressure overload myocardial hypertrophy induced by abdominal aorta ligation (AB) and cultured neonatal rat cardiomyocytes.

Intervention

Overexpression of miR-142-3p via miR-142-3p agomir injected into the tail vein at 2 and 4 weeks (in vivo) and miR-142-3p mimic (in vitro).

Comparator

Abdominal aorta ligation without miR-142-3p agomir (in vivo) and AngII treatment with miRNA mimic nc (in vitro).

Outcome

Cardiac hypertrophy (assessed by echocardiography, HE staining, ANP, BNP, and β-MHC mRNA expression) and mitochondrial function (assessed by membrane potential, mitochondrial density, and oxygen consumption rate).surrogate

Overexpression of miR-142-3p mitigates cardiac hypertrophy and preserves mitochondrial function by inhibiting SH2B1 expression in preclinical models.

Cite This Study

Liu et al. (2018) studied Cardiac hypertrophy. miR-142-3p overexpression vs. Pressure overload/AngII without miR-142-3p overexpression was evaluated on Cardiac hypertrophy and mitochondrial function. Overexpression of miR-142-3p mitigated cardiac hypertrophy and protected mitochondrial function in vitro and in vivo by directly inhibiting SH2B1 expression.

synapsesocial.com/papers/6a9d7ebb34685bd7702a0727 https://doi.org/10.1016/j.biopha.2018.09.146

Topics

Heart failure HFrEF treatment

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October 4, 2018Biomedicine & PharmacotherapyOpen Access

Overexpression of miR-142-3p improves mitochondrial function in cardiac hypertrophy

View Full Paper

Ask AI

Bookmark

Key result

Overexpression of miR-142-3p mitigated cardiac hypertrophy and protected mitochondrial function in vitro and in vivo by directly inhibiting SH2B1 expression.

Why the study?

Does overexpression of miR-142-3p mitigate cardiac hypertrophy and improve mitochondrial function in preclinical models?

Population

Rat model of pressure overload myocardial hypertrophy induced by abdominal aorta ligation and cultured…

Comparison

Overexpression of miR-142-3p via miR-142-3p… vs Abdominal aorta ligation without miR-142-3p…

Design

Preclinical

Follow-up

4 weeks (in vivo)

Authors

BLBeilei LiuShanghai Jiao Tong University MCMian ChengTongji Hospital SHShan HuChina Automotive Engineering Research Institute

Discussion

Member takes

Implication

Hypothesis-generating for miR-142-3p in hypertrophy; leaves open human translation and trials.

Structured PICO

Does overexpression of miR-142-3p mitigate cardiac hypertrophy and improve mitochondrial function in preclinical models?

Population

Rat model of pressure overload myocardial hypertrophy induced by abdominal aorta ligation (AB) and cultured neonatal rat cardiomyocytes.

Intervention

Overexpression of miR-142-3p via miR-142-3p agomir injected into the tail vein at 2 and 4 weeks (in vivo) and miR-142-3p mimic (in vitro).

Comparator

Abdominal aorta ligation without miR-142-3p agomir (in vivo) and AngII treatment with miRNA mimic nc (in vitro).

Outcome

Overexpression of miR-142-3p mitigates cardiac hypertrophy and preserves mitochondrial function by inhibiting SH2B1 expression in preclinical models.

Cite This Study

synapsesocial.com/papers/6a9d7ebb34685bd7702a0727 https://doi.org/10.1016/j.biopha.2018.09.146

Also Consider

Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context:

Topics

Heart failure HFrEF treatment

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