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

Clinically applicable antianginal agents suppress osteoblastic transformation of myogenic cells and heterotopic ossifications in mice.

Journal of bone and mineral metabolism - 1 Jan 2013

Yamamoto Ryuichiro, Matsushita Masaki, Kitoh Hiroshi, Masuda Akio, Ito Mikako, Katagiri Takenobu, Kawai Tatsushi, Ishiguro Naoki, Ohno Kinji

Abstract excerpt

Fibrodysplasia ossificans progressiva (FOP) is a rare autosomal dominant disorder characterized by progressive heterotopic ossification. FOP is caused by a gain-of-function mutation in ACVR1 encoding the bone morphogenetic protein type II receptor, ACVR1/ALK2. The mutant receptor causes upregulation of a transcriptional factor, Id1. No therapy is available to prevent the progressive heterotopic ossification in...

Read the complete abstract on PubMed

Topics

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

Share to Activin Receptors, Type I
Share to Bone Morphogenetic Protein 2

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Calcium Channel Blockers

Share to Drug Evaluation, Preclinical

Share to Muscle Cells

Share to Myositis Ossificans

Share to Ossification, Heterotopic

Share to Smad Proteins

Source

Identifiers

PMID: 23011467
DOI: 10.1007/s00774-012-0380-2

Genes

ACVR1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Clinically applicable antianginal agents suppress osteoblastic transformation of myogenic cells and heterotopic ossifications in mice.PMID 23011467Read ↗

From mysteries to medicines: drug development for fibrodysplasia ossificans progressivaSemantic proximity Read ↗

An mTOR Signaling Modulator Suppressed Heterotopic Ossification of Fibrodysplasia Ossificans ProgressivaSemantic proximity Read ↗

Clinical Aspects and Current Therapeutic Approaches for FOPSemantic proximity Read ↗

An anti-ACVR1 antibody exacerbates heterotopic ossification by fibro/adipogenic progenitors in fibrodysplasia ossificans progressiva miceSemantic proximity Read ↗

Recent progress in drug development for fibrodysplasia ossificans progressiva.Semantic proximity Read ↗

Challenges and Opportunities for Drug Repositioning in Fibrodysplasia Ossificans ProgressivaSemantic proximity Read ↗

Palovarotene Inhibits Heterotopic Ossification and Maintains Limb Mobility and Growth in Mice With the Human ACVR1(R206H) Fibrodysplasia Ossificans Progressiva (FOP) Mutation.Semantic proximity Read ↗

The Horizon of a Therapy for Rare Genetic Diseases: A “Druggable” Future for Fibrodysplasia Ossificans ProgressivaSemantic proximity Read ↗

High-throughput screening for modulators of <i>ACVR1</i> transcription: discovery of potential therapeutics for fibrodysplasia ossificans progressivaSemantic proximity Read ↗

A new era for fibrodysplasia ossificans progressiva: a druggable target for the second skeleton.Semantic proximity Read ↗

iMSC-mediated delivery of ACVR2B-Fc fusion protein reduces heterotopic ossification in a mouse model of fibrodysplasia ossificans progressiva.Semantic proximity Read ↗

An anti-ACVR1 antibody exacerbates heterotopic ossification by fibro-adipogenic progenitors in fibrodysplasia ossificans progressiva mice.Semantic proximity Read ↗

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