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

Subcellular Remodeling in Filamin C Deficient Mouse Hearts Impairs Myocyte Tension Development during Progression of Dilated Cardiomyopathy.

International journal of molecular sciences - 14 Jan 2022

Powers Joseph D, Kirkland Natalie J, Liu Canzhao, Razu Swithin S, Fang Xi, Engler Adam J, Chen Ju, McCulloch Andrew D

Abstract excerpt

Dilated cardiomyopathy (DCM) is a life-threatening form of heart disease that is typically characterized by progressive thinning of the ventricular walls, chamber dilation, and systolic dysfunction. Multiple mutations in the gene encoding filamin C (FLNC), an actin-binding cytoskeletal protein in cardiomyocytes, have been found in patients with DCM. However, the mechanisms that lead to contractile impairment and...

Read the complete abstract on PubMed

Topics

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

Share to Biomarkers
Share to Calcium

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Calcium Signaling

Share to Cardiomyopathy, Dilated

Share to Filamins

Share to Mice, Knockout

Share to Myocardial Contraction

Share to Myocytes, Cardiac

Source

Open in PubMed Open full text

Identifiers

PMID: 35055055
DOI: 10.3390/ijms23020871
PMCID: PMC8779483

Genes

FLNC

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Subcellular Remodeling in Filamin C Deficient Mouse Hearts Impairs Myocyte Tension Development during Progression of Dilated Cardiomyopathy.PMID 35055055Read ↗

Novel Mutation in FLNC (Filamin C) Causes Familial Restrictive Cardiomyopathy.Semantic proximity Read ↗

Filamin C in cardiomyopathy: from physiological roles to DNA variants.Semantic proximity Read ↗

Filamin C Deficiency Impairs Sarcomere Stability and Activates Focal Adhesion Kinase through PDGFRA Signaling in Induced Pluripotent Stem Cell-Derived CardiomyocytesSemantic proximity Read ↗

Cardiac Filaminopathies: Illuminating the Divergent Role of Filamin C Mutations in Human CardiomyopathySemantic proximity Read ↗

Interaction of Filamin C With Actin Is Essential for Cardiac Development and Function.Semantic proximity Read ↗

Myofibrillar instability exacerbated by acute exercise in filaminopathy.Semantic proximity Read ↗

Filamin C Truncation Mutations Are Associated With Arrhythmogenic Dilated Cardiomyopathy and Changes in the Cell-Cell Adhesion Structures.Semantic proximity Read ↗

Dilated cardiomyopathy mutations in thin-filament regulatory proteins reduce contractility, suppress systolic Ca2+, and activate NFAT and Akt signaling.Semantic proximity Read ↗

Filamin C is a highly dynamic protein associated with fast repair of myofibrillar microdamage.Semantic proximity Read ↗

Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programsSemantic proximity Read ↗

Mechanosensitive Gene Regulation by Myocardin-Related Transcription Factors Is Required for Cardiomyocyte Integrity in Load-Induced Ventricular HypertrophySemantic proximity Read ↗

Novel pathogenic variants in filamin C identified in pediatric restrictive cardiomyopathySemantic proximity Read ↗

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