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February 18, 2015Cardiovascular ResearchOpen Access

Lack of collagen VIII reduces fibrosis and promotes early mortality and cardiac dilatation in pressure overload in mice†

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Population

colVIII knock-out mice and wild type mice subjected to aortic banding to induce pressure overload; neonatal…

Comparison

Collagen VIII knock-out (col8KO) vs Wild type (WT) mice

Design

Preclinical

Follow-up

Up to 56 days

Key result

Collagen VIII knock-out in mice subjected to pressure overload promoted early mortality at 3-9 days and left ventricular dilatation while reducing myofibroblast differentiation and fibrosis.

Authors

BSBiljana SkrbicKEKristin V. T. EngebretsenMSMari E. Strand

Discussion

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Overview

Findings in mice caution against fibrosis reduction without preserving adaptive remodeling; leaves open collagen VIII as a target in pressure-overload states.

Structured PICO

P
Population
Mice subjected to aortic banding to study the role of collagen VIII in pressure overload-induced remodeling.
E
Exposure
Collagen VIII knock-out (col8KO)
C
Comparator
Wild type (WT) mice
O
Outcome
Mortality and left ventricular (LV) dilatation following aortic bandingsurrogate

Lack of collagen VIII in mice reduces fibrosis but promotes early mortality and left ventricular dilatation in response to pressure overload, highlighting its role in adaptive remodeling.

Cite This Study

Skrbic et al. (2015) studied Pressure overload-induced remodelling. Collagen VIII knock-out (col8KO) vs. Wild type (WT) mice was evaluated on Mortality and left ventricular dilatation. Collagen VIII knock-out in mice subjected to pressure overload promoted early mortality at 3-9 days and left ventricular dilatation while reducing myofibroblast differentiation and fibrosis.

synapsesocial.com/papers/6a6c62fd547974b2dbf491d6https://doi.org/10.1093/cvr/cvv041
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