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January 13, 2015Cardiovascular ResearchOpen Access

Syndecan-4 is a key determinant of collagen cross-linking and passive myocardial stiffness in the pressure-overloaded heart

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Why the study?

Does syndecan-4 mediate collagen cross-linking and myocardial stiffening in pressure-overloaded hearts?

Population

syndecan-4(-/-) mice and wild-type mice subjected to aortic banding (AB), and cardiac fibroblasts

Comparison

syndecan-4 knockout (syndecan-4) and in vitro… vs Wild-type mice or control fibroblasts

Design

Preclinical

Key result

Syndecan-4 promotes collagen cross-linking and myocardial stiffening in the pressure-overloaded heart via both its cytosolic domain (NFAT signaling) and extracellular domain.

Authors

KHKate M. HerumILIda G. LundeBSBiljana Skrbic

Discussion

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Member takes

Overview

Should not yet change clinical practice in pressure overload; hypothesis-generating for dual-domain syndecan-4 targeting.

Structured PICO

Does syndecan-4 mediate collagen cross-linking and myocardial stiffening in pressure-overloaded hearts?

P
Population
syndecan-4(-/-) mice and wild-type mice subjected to aortic banding (AB), and cardiac fibroblasts
I
Intervention
syndecan-4 knockout (syndecan-4(-/-)) and in vitro manipulation (overexpression/inhibition)
C
Comparator
Wild-type mice or control fibroblasts
O
Outcome
Passive tension of left ventricular muscle strips and collagen cross-linkingsurrogate

Syndecan-4 plays a dual role in promoting collagen cross-linking and myocardial stiffening during pressure overload via NFAT signaling and extracellular domain interactions.

Cite This Study

Herum et al. (2015) studied Diastolic dysfunction and pressure-overloaded heart. Aortic banding (AB) in syndecan-4(-/-) mice vs. Wild-type mice was evaluated on Passive tension of left ventricular muscle strips and collagen cross-linking. Syndecan-4 promotes collagen cross-linking and myocardial stiffening in the pressure-overloaded heart via both its cytosolic domain (NFAT signaling) and extracellular domain.

synapsesocial.com/papers/6a092c8fa419c5e264d2621bhttps://doi.org/10.1093/cvr/cvv002
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