ArticleCirculation. Heart failure2020
Nexilin Is Necessary for Maintaining the Transverse-Axial Tubular System in Adult Cardiomyocytes.
Article in Circulation. Heart failure, 2020. 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, 35 citations in OpenAlex.
- Cardiac Cell Remodeling in Obesity and Diabetes.Handbook of experimental pharmacology · 2026Review
- Integrating transcriptome and proteome profiles to compare carcass and meat quality traits between Songliao and Songlei black pigs.Frontiers in nutrition · 2026Article
- Calcium handling remodeling in dilated cardiomyopathy: From molecular mechanisms to targeted therapies.Channels (Austin, Tex.) · 2025Review
- Exploring the Nexus of Genotype and Phenotype in Nexilin-Related Genetic Cardiomyopathy.JACC. Heart failure · 2025Article
- Genetic and Phenotypic Characterization of Nexilin (NEXN)-Related Cardiomyopathy: Results From a Multicentric Study.JACC. Heart failure · 2025Article
- NEXN protects against vascular calcification by promoting SERCA2 SUMOylation and stabilization.Nature communications · 2025Article
- NEXN deficiency leads to dilated cardiomyopathy in human pluripotent stem cell-derived cardiomyocytes.Stem cell research & therapy · 2025Article
- NEXN regulates vascular smooth muscle cell phenotypic switching and neointimal hyperplasia.JCI insight · 2025Article
- Computational analysis of congenital heart disease associated SNPs: unveiling their impact on the gene regulatory system.BMC genomics · 2025Article
- Article
- Unveiling the Spectrum of Minor Genes in Cardiomyopathies: A Narrative Review.International journal of molecular sciences · 2024Review
- Biallelic NEXN variants and fetal onset dilated cardiomyopathy: two independent case reports and revision of literature.Italian journal of pediatrics · 2024Review
- Pediatric dilated cardiomyopathy: a review of current clinical approaches and pathogenesis.Frontiers in pediatrics · 2024Review
- Endoplasmic Reticulum-Plasma Membrane Junctions as Sites of Depolarization-Induced CaAnnual review of physiology · 2023Review
- Structural and signaling proteins in the Z-disk and their role in cardiomyopathies.Frontiers in physiology · 2023Review
- Sarcomere maturation: function acquisition, molecular mechanism, and interplay with other organelles.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Review
- Loss of Nexilin function leads to a recessive lethal fetal cardiomyopathy characterized by cardiomegaly and endocardial fibroelastosis.American journal of medical genetics. Part A · 2022Article
- Understanding the molecular basis of cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2022Review
- Subcellular Remodeling in Filamin C Deficient Mouse Hearts Impairs Myocyte Tension Development during Progression of Dilated Cardiomyopathy.International journal of molecular sciences · 2022Article
- Structure-function relationships and modifications of cardiac sarcoplasmic reticulum Ca2+-transport.Physiological research · 2021Review
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundNEXN (nexilin) is a protein of the junctional membrane complex required for development of cardiac T-tubules. Global and cardiomyocyte-specific loss of
methods
resultsInducible cardiomyocyte-specific loss of
conclusionsResults here reported reveal NEXN to be a pivotal component of adult junctional membrane complexes required for maintenance of transverse-axial tubular architecture. These results demonstrate that NEXN plays an essential role in the adult cardiomyocyte and give further understanding of pathological mechanisms responsible for cardiomyopathy in patients carrying mutations in the NEXN gene.
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Registered trials
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.