What does this research mean for the field?

Overexpression of Ankrd1 exacerbates pathological cardiac dysfunction by enhancing cardiomyocyte apoptosis mediated through the up-regulation of p53 in rodents. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

December 16, 2014Clinical Science

Overexpression of ankyrin repeat domain 1 enhances cardiomyocyte apoptosis by promoting p53 activation and mitochondrial dysfunction in rodents

Q: What is the clinical evidence from this study?

Population: Heart failure / pressure overload. Intervention: Ad-Ankrd1 (Ankrd1 overexpression) vs. Ankrd1 knockdown / control. Primary outcome: Cardiomyocyte apoptosis and cardiac dysfunction.

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Key result

Overexpression of Ankrd1 exacerbated pathological cardiac dysfunction through enhancement of cardiomyocyte apoptosis mediated by the up-regulation of p53 in rodents.

Population

Neonatal rat cardiomyocytes and mice with pressure overload induced by transverse aortic constriction

Comparison

Overexpression of Ankrd1 via recombinant… vs Control conditions (implied)

Design

Preclinical

Authors

LSLiang ShenBeijing Institute of Technology CCChun‐I ChenGuangdong University of Technology XWXuan WeiHong Kong University of Science and Technology

Discussion

Member takes

Implication

Hypothesis-generating for Ankrd1-p53 targeting in HF; leaves open translation from rodent models to humans.

Structured PICO

Population

Neonatal rat cardiomyocytes (NRCs) and mice with pressure overload induced by transverse aortic constriction (TAC)

Intervention

Overexpression of Ankrd1 via recombinant adenovirus (Ad-Ankrd1) or knockdown/silencing of Ankrd1

Comparator

Control conditions (implied)

Outcome

Cardiomyocyte apoptosis, mitochondrial dysfunction, and cardiac dysfunction (lung weight/body weight ratio, left ventricular fractional shortening)surrogate

Ankrd1 overexpression exacerbates pathological cardiac dysfunction by promoting p53-mediated cardiomyocyte apoptosis in rodent models of pressure overload.

Cite This Study

Shen et al. (2014) studied Heart failure / pressure overload. Ad-Ankrd1 (Ankrd1 overexpression) vs. Ankrd1 knockdown / control was evaluated on Cardiomyocyte apoptosis and cardiac dysfunction. Overexpression of Ankrd1 exacerbated pathological cardiac dysfunction through enhancement of cardiomyocyte apoptosis mediated by the up-regulation of p53 in rodents.

synapsesocial.com/papers/6a18cfd90048a5c8b24ae91c https://doi.org/10.1042/cs20140586

Topics

Heart failure HFrEF treatment

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Overexpression of ankyrin repeat domain 1 enhances cardiomyocyte apoptosis by promoting p53 activation and mitochondrial dysfunction in rodents

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Topics

Overexpression of ankyrin repeat domain 1 enhances cardiomyocyte apoptosis by promoting p53 activation and mitochondrial dysfunction in rodents

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Topics

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