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

Smad3 signaling critically regulates fibroblast phenotype and function in healing myocardial infarction.

Circulation research - 6 Aug 2010

Dobaczewski Marcin, Bujak Marcin, Li Na, Gonzalez-Quesada Carlos, Mendoza Leonardo H, Wang Xiao-Fan, Frangogiannis Nikolaos G

Abstract excerpt

RATIONALE: Cardiac fibroblasts are key effector cells in the pathogenesis of cardiac fibrosis. Transforming growth factor (TGF)-beta/Smad3 signaling is activated in the border zone of healing infarcts and induces fibrotic remodeling of the infarcted ventricle contributing to the development of diastolic dysfunction. OBJECTIVE: The present study explores the mechanisms responsible for the fibrogenic effects of...

Read the complete abstract on PubMed

Topics

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

Share to Extracellular Matrix Proteins
Share to Myocardial Contraction

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Share to Myocardial Infarction

Share to Smad3 Protein

Share to Trans-Activators

Share to Transforming Growth Factor beta1

Share to Up-Regulation

Share to Wound Healing

Source

Open in PubMed Open full text

Identifiers

PMID: 20522804
DOI: 10.1161/CIRCRESAHA.109.216101
PMCID: PMC2917472

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Smad3 signaling critically regulates fibroblast phenotype and function in healing myocardial infarction.PMID 20522804Read ↗

Differential effects of Smad2 and Smad3 in regulation of macrophage phenotype and function in the infarcted myocardium.Semantic proximity Read ↗

Fibroblast-specific TGF-β–Smad2/3 signaling underlies cardiac fibrosisSemantic proximity Read ↗

Cardiac fibroblast GSK-3α mediates adverse myocardial fibrosis via IL-11 and ERK pathwaySemantic proximity Read ↗

Deletion of Smad3 Protects Against Diabetic Myocardiopathy in db/db Mice Semantic proximity Read ↗

Fibroblast polarization over the myocardial infarction time continuum shifts roles from inflammation to angiogenesisSemantic proximity Read ↗

The Role of the TGF-β Superfamily in Myocardial InfarctionSemantic proximity Read ↗

Deletion of delta-like 1 homologue accelerates fibroblast–myofibroblast differentiation and induces myocardial fibrosisSemantic proximity Read ↗

Fibulin-3 is necessary to prevent cardiac rupture following myocardial infarctionSemantic proximity Read ↗

Emerging therapeutic targets for cardiac arrhythmias: role of STAT3 in regulating cardiac fibroblast functionSemantic proximity Read ↗

Changes in cardiac resident fibroblast physiology and phenotype in aging.Semantic proximity Read ↗

The novel cardiokine GDF3 predicts adverse fibrotic remodeling post-myocardial infarctionSemantic proximity Read ↗

The extracellular matrix modulates fibroblast phenotype and function in the infarcted myocardium.Semantic proximity Read ↗

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