What is the clinical evidence from this study?

Study design: Other. Population: Adult cardiac conduction disease. Intervention: Prox1 haploinsufficiency vs. Nkx2.5(Cre/+) controls. Primary outcome: Rescue of hemodynamic parameters, anatomy, and atrioventricular conduction.

May 30, 2012Circulation ResearchOpen Access

Prox1 haploinsufficiency rescued Nkx2.5 conduction disease phenotypes, normalizing atrioventricular conduction and anatomy in a mouse model via a Prox1-HDAC3-Nkx2.5 signaling pathway.

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Population

Mouse models including Nkx2.5; Prox1 animals, Nkx2.5 controls, and Prox1 heterozygous mice on a Cx40…

Comparison

Prox1 haploinsufficiency vs Nkx2.5(Cre/+) controls

Design

Preclinical

Key result

Prox1 haploinsufficiency rescued Nkx2.5 conduction disease phenotypes, normalizing atrioventricular conduction and anatomy in a mouse model via a Prox1-HDAC3-Nkx2.5 signaling pathway.

Authors

CRCatherine A. Risebro LPLouisa K. Petchey NSNicola Smart

Discussion

Member takes

Overview

Hypothesis-generating for Prox1 modulation in human conduction disease; requires validation beyond mouse models before any clinical consideration.

Structured PICO

Population

Mouse models including Nkx2.5(Cre/+); Prox1(loxP/+) animals, Nkx2.5(Cre/+) controls, and Prox1 heterozygous mice on a Cx40(EGFP) background

Intervention

Prox1 haploinsufficiency (Cre-mediated knock-down of Prox1)

Comparator

Nkx2.5(Cre/+) controls

Outcome

Hemodynamic parameters, anatomy of the atrioventricular node and His-Purkinje network, atrioventricular conduction, and excitation-contractionsurrogate

Prox1 recruits HDAC3 to directly repress Nkx2.5, and Prox1 haploinsufficiency rescues Nkx2.5-dependent adult cardiac conduction disease phenotypes in a mouse model.

Cite This Study

Risebro et al. (2012) studied Adult cardiac conduction disease. Prox1 haploinsufficiency vs. Nkx2.5(Cre/+) controls was evaluated on Rescue of hemodynamic parameters, anatomy, and atrioventricular conduction. Prox1 haploinsufficiency rescued Nkx2.5 conduction disease phenotypes, normalizing atrioventricular conduction and anatomy in a mouse model via a Prox1-HDAC3-Nkx2.5 signaling pathway.

synapsesocial.com/papers/6a71e1a35d37378ac1dee23e https://doi.org/10.1161/circresaha.111.260695

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May 30, 2012Circulation ResearchOpen Access

Prox1 haploinsufficiency rescued Nkx2.5 conduction disease phenotypes, normalizing atrioventricular conduction and anatomy in a mouse model via a Prox1-HDAC3-Nkx2.5 signaling pathway.

View Full Paper

Ask AI

Bookmark

Population

Mouse models including Nkx2.5; Prox1 animals, Nkx2.5 controls, and Prox1 heterozygous mice on a Cx40…

Comparison

Prox1 haploinsufficiency vs Nkx2.5(Cre/+) controls

Design

Preclinical

Key result

Prox1 haploinsufficiency rescued Nkx2.5 conduction disease phenotypes, normalizing atrioventricular conduction and anatomy in a mouse model via a Prox1-HDAC3-Nkx2.5 signaling pathway.

Authors

CRCatherine A. Risebro LPLouisa K. Petchey NSNicola Smart

Discussion

Member takes

Overview

Hypothesis-generating for Prox1 modulation in human conduction disease; requires validation beyond mouse models before any clinical consideration.

Structured PICO

Population

Mouse models including Nkx2.5(Cre/+); Prox1(loxP/+) animals, Nkx2.5(Cre/+) controls, and Prox1 heterozygous mice on a Cx40(EGFP) background

Intervention

Prox1 haploinsufficiency (Cre-mediated knock-down of Prox1)

Comparator

Nkx2.5(Cre/+) controls

Outcome

Hemodynamic parameters, anatomy of the atrioventricular node and His-Purkinje network, atrioventricular conduction, and excitation-contractionsurrogate

Prox1 recruits HDAC3 to directly repress Nkx2.5, and Prox1 haploinsufficiency rescues Nkx2.5-dependent adult cardiac conduction disease phenotypes in a mouse model.

Cite This Study

synapsesocial.com/papers/6a71e1a35d37378ac1dee23e https://doi.org/10.1161/circresaha.111.260695

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