ReviewHeart failure reviews2022
Filamin C in cardiomyopathy: from physiological roles to DNA variants.
Review in Heart failure reviews, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 48 citations in OpenAlex.
- Filamin C Genetic Cardiomyopathy Presenting as Acute Myocardial Injury.JACC. Case reports · 2026Article
- Unusual hypertrophic cardiomyopathy with severe right ventricular outflow tract obstruction and two septal aneurysms: a case report.BMC cardiovascular disorders · 2026Article
- Genetic Spectrum, Clinical Characteristics, and Molecular Pathogenesis of Hypertrophic Cardiomyopathy Requiring Heart Transplantation.Journal of cardiovascular development and disease · 2025Article
- The Expanding Genetic Architecture of Arteriopathies: From Canonical TAAD Genes to Emerging Connective Tissue and Signaling Pathways.Medical sciences (Basel, Switzerland) · 2025Review
- Effect of Mutations in the C-Terminal 22-24 Domains of Filamin C Associated with Cardio- and Myopathies on Its Interaction with Small Heat Shock Protein HspB7.International journal of molecular sciences · 2025Article
- Protein Disulfide Isomerase Involvement in Dilated Cardiomyopathy Caused by Filamin C Deficiency in Male Mice.Journal of cellular and molecular medicine · 2025Article
- Distinct molecular features of FLNC mutations, associated with different clinical phenotypes.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Dilated Cardiomyopathy in a Young Patient With anCase reports in medicine · 2025Article
- Pathomechanisms of Monoallelic variants in TTN causing skeletal muscle disease.Human molecular genetics · 2024Article
- Risk Assessment and Personalized Treatment Options in Inherited Dilated Cardiomyopathies: A Narrative Review.Biomedicines · 2024Review
- Exploring TTN variants as genetic insights into cardiomyopathy pathogenesis and potential emerging clues to molecular mechanisms in cardiomyopathies.Scientific reports · 2024Review
- Differential sensitivity to longitudinal and transverse stretch mediates transcriptional responses in mouse neonatal ventricular myocytes.American journal of physiology. Heart and circulatory physiology · 2024Article
- TheBiomedicines · 2024Article
- Identification of a Missense Mutation in theJournal of multidisciplinary healthcare · 2024Article
- FLNC Associated Restrictive Cardiomyopathy and Hypertrabeculation, a Rare Association.Arquivos brasileiros de cardiologia · 2024Article
- Genetic characterization of dilated cardiomyopathy patients undergoing heart transplantation in the Chinese population by whole-exome sequencing.Journal of translational medicine · 2023Article
- Force-Dependent Structural Changes of Filamin C Rod Domains Regulated by Filamin C Dimer.Journal of the American Chemical Society · 2023Article
- Characterization of serotonin-5-HTR1E signaling pathways and its role in cell survival.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Pressure overload induces ISG15 to facilitate adverse ventricular remodeling and promote heart failure.The Journal of clinical investigation · 2023Article
- Characterization of serotonin-5-HTR1E signaling pathways and its role in cell survival.Research square · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiomyopathy affects approximately 1 in 500 adults and is the leading cause of death. Familial cases are common, and mutations in many genes are involved in cardiomyopathy, especially those in genes encoding cytoskeletal, sarcomere, and nuclear envelope proteins. Filamin C is an actin-binding protein encoded by filamin C (FLNC) gene and participates in sarcomere stability maintenance. FLNC was first demonstrated to be a causal gene of myofibrillar myopathy; recently, it has been found that FLNC mutation plays a critical role in the pathogenesis of cardiomyopathy. In this review, we summarized the physiological roles of filamin C in cardiomyocytes and the genetic evidence for links between FLNC mutations and cardiomyopathies. Truncated FLNC is enriched in dilated cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Non-truncated FLNC is enriched in hypertrophic cardiomyopathy and restrictive cardiomyopathy. Two major pathomechanisms in FLNC-related cardiomyopathy have been described: protein aggregation resulting from non-truncating mutations and haploinsufficiency triggered by filamin C truncation. Therefore, it is important to understand the cellular biology and molecular regulation of FLNC to design new therapies to treat patients with FLNC-related cardiomyopathy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.