Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Syndecan-4 deficiency accelerates the transition from compensated hypertrophy to heart failure following pressure overload.

Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology - 1 Jan 2000

Li Guannan, Xie Jun, Chen Jianzhou, Li Ran, Wu Han, Zhang Xinlin, Chen Qinhua, Gu Rong, Xu Biao

Abstract excerpt

Increasing evidence suggests that a mismatch between angiogenesis and myocardial growth contributes to the transition from adaptive cardiac hypertrophy to heart failure following pressure overload. Syndecan-4 is a transmembrane proteoglycan that binds to growth factors and extracellular matrix proteins and is critical in focal adhesion formation. However, its effects on coronary angiogenesis during pressure...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aorta
Share to Arterial Pressure

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cardiomegaly

Share to Ligation

Share to Neovascularization, Physiologic

Share to Protein Kinase C-alpha

Share to Ventricular Function, Left

Share to Ventricular Remodeling

Source

Identifiers

PMID: 28395201
DOI: 10.1016/j.carpath.2017.03.008

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Syndecan-4 deficiency accelerates the transition from compensated hypertrophy to heart failure following pressure overload.PMID 28395201Read ↗

Bone Morphogenetic Protein-4 Mediates Cardiac Hypertrophy, Apoptosis, and Fibrosis in Experimentally Pathological Cardiac HypertrophySemantic proximity Read ↗

Cardiac growth and angiogenesis coordinated by intertissue interactionsSemantic proximity Read ↗

Angiogenesis and angiocrines regulating heart growthSemantic proximity Read ↗

Differential cardiac hypertrophy and signaling pathways in pressure versus volume overload.Semantic proximity Read ↗

Fibroblast GATA-4 and GATA-6 promote myocardial adaptation to pressure overload by enhancing cardiac angiogenesisSemantic proximity Read ↗

Tenascin-C promotes chronic pressure overload-induced cardiac dysfunction, hypertrophy and myocardial fibrosis.Semantic proximity Read ↗

Endogenous thrombospondin 1 protects the pressure-overloaded myocardium by modulating fibroblast phenotype and matrix metabolism.Semantic proximity Read ↗

Therapeutic inhibition of the miR-34 family attenuates pathological cardiac remodeling and improves heart functionSemantic proximity Read ↗

Endothelial deletion of protein tyrosine phosphatase-1B protects against pressure overload-induced heart failure in mice.Semantic proximity Read ↗

Rapamycin attenuates pathological hypertrophy caused by an absence of trabecular formation.Semantic proximity Read ↗

Macrophage-derived CCL24 promotes fibrosis and worsens cardiac dysfunction during heart failureSemantic proximity Read ↗

Syndecan-2 is essential for angiogenic sprouting during zebrafish development.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.