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October 20, 2016Proceedings of the National Academy of SciencesOpen Access

PDE1C deficiency antagonizes pathological cardiac remodeling and dysfunction

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Why the study?

Does PDE1C deficiency or inhibition prevent pathological cardiac remodeling and dysfunction in preclinical models?

Population

Mouse models subjected to transverse aortic constriction, adult mouse cardiac myocytes, and human failing…

Comparison

PDE1C deficiency or pharmacological inhibition vs Wild-type mice or untreated controls

Design

Preclinical

Authors

WKWalter E. KnightUniversity of Colorado Anschutz Medical CampusSCSi ChenShenzhen Third People’s HospitalYZYishuai ZhangFirst Affiliated Hospital of Xi'an Jiaotong University

Discussion

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Overview

PDE1C inhibition may attenuate remodeling in pressure overload; leaves open translation to human HF.

Structured PICO

Does PDE1C deficiency or inhibition prevent pathological cardiac remodeling and dysfunction in preclinical models?

P
Population
Mouse models (PDE1C-knockout and wild-type) subjected to transverse aortic constriction, adult mouse cardiac myocytes, and human failing heart samples.
I
Intervention
PDE1C deficiency (genetic knockout) or pharmacological inhibition
C
Comparator
Wild-type mice or untreated controls
O
Outcome
Pathological cardiac remodeling and dysfunction (including myocardial hypertrophy, apoptosis, cardiac fibrosis, and loss of contractile function)surrogate

PDE1C deficiency protects against pathological cardiac remodeling and dysfunction in mice, highlighting PDE1C as a potential therapeutic target for heart failure.

Cite This Study

Knight et al. (2016) studied this question.

synapsesocial.com/papers/6a714c45febe604dd709fd71https://doi.org/10.1073/pnas.1607728113
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