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

A time course investigation of the statin paradox among valvular interstitial cell phenotypes.

American journal of physiology. Heart and circulatory physiology - 1 Oct 2012

Monzack Elyssa L, Masters Kristyn S

Abstract excerpt

Statin drugs are prescribed primarily for their ability to lower cholesterol, but may also exert beneficial side effects unrelated to cholesterol metabolism. Previous work has described a "statin paradox," where statin treatment decreased osteoblastic markers in valve myofibroblasts while increasing those same markers in preosteoblasts. However, valvular interstitial cells (VICs) themselves are a multipotent cell...

Read the complete abstract on PubMed

Topics

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

Share to Alkaline Phosphatase
Share to Aortic Valve
Share to Hydroxymethylglutaryl-CoA Reductase Inhibitors

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Myofibroblasts

Share to Osteoblasts

Share to Osteocalcin

Share to Osteogenesis

Share to Simvastatin

Source

Open in PubMed Open full text

Identifiers

PMID: 22904157
DOI: 10.1152/ajpheart.00263.2012
PMCID: PMC3469700

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A time course investigation of the statin paradox among valvular interstitial cell phenotypes.PMID 22904157Read ↗

Cell Phenotype Transitions in Cardiovascular CalcificationSemantic proximity Read ↗

Leptin induces osteoblast differentiation of human valvular interstitial cells via the Akt and ERK pathways.Semantic proximity Read ↗

Patient-Derived Circulating Monocytes Promote Calcific Aortic Valve Disease ProgressionSemantic proximity Read ↗

Sex-related differences in gene expression by porcine aortic valvular interstitial cells.Semantic proximity Read ↗

Simulation of early calcific aortic valve disease in a 3D platform: A role for myofibroblast differentiation.Semantic proximity Read ↗

Shared gene expression profiles in developing heart valves and osteoblast progenitor cellsSemantic proximity Read ↗

Altered MicroRNA Expression Is Responsible for the Pro-Osteogenic Phenotype of Interstitial Cells in Calcified Human Aortic Valves.Semantic proximity Read ↗

Mitral valve endothelial cells with osteogenic differentiation potential.Semantic proximity Read ↗

Role of the Rho pathway in regulating valvular interstitial cell phenotype and nodule formation.Semantic proximity Read ↗

Proteomic analysis of interstitial aortic valve cells acquiring a pro-calcific profile.Semantic proximity Read ↗

Parathyroid Hormone Induces Human Valvular Endothelial Cells Dysfunction That Impacts the Osteogenic Phenotype of Valvular Interstitial Cells.Semantic proximity Read ↗

Similar, but not the same: multi-omics comparison of human valve interstitial cells and osteoblast osteogenic differentiation expanded with an estimation of data-dependent and data-independent PASEFSemantic proximity Read ↗

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