ArticleNature communications2018
NF-κB inhibition rescues cardiac function by remodeling calcium genes in a Duchenne muscular dystrophy model.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 45 citations in OpenAlex.
- Perioperative assessment of muscle inflammation susceptibility in patients with end-stage osteoarthritis.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Trial
- Treatment with the Nox1/4 inhibitor Setanaxib ameliorates cardiac function in mouse models of Duchenne muscular dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Comparative transcriptomics analysis of histone deacetylases, transcription factors, and ion channel genes in human iPSC-cardiomyocytes vs. the adult human heart.Journal of precision medicine (Amsterdam, Netherlands) · 2026Article
- Comparative transcriptomics analysis of histone deacetylases, transcription factors, and ion channel genes in human iPSC-cardiomyocytes vs. the adult human heart.bioRxiv : the preprint server for biology · 2026Article
- Klotho Is Cardioprotective in the mdx Mouse Model of Duchenne Muscular Dystrophy.The American journal of pathology · 2025Article
- Novel oral compound Z526 mitigates cancer-associated cachexia via intervening NF-κB signaling and oxidative stress.Genes & diseases · 2025Article
- Striking Cardioprotective Effects of an Adiponectin Receptor Agonist in an Aged Mouse Model of Duchenne Muscular Dystrophy.Antioxidants (Basel, Switzerland) · 2024Article
- Investigating the NF-κB signaling pathway in heart failure: Exploring potential therapeutic approaches.Heliyon · 2024Review
- Lipin1 as a therapeutic target for respiratory insufficiency of duchenne muscular dystrophy.Frontiers in physiology · 2024Article
- RANKL Inhibition Reduces Cardiac Hypertrophy inCells · 2023Article
- Epigenetic Regulation of Macrophage Polarization in Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Human iPSC-Cardiomyocytes as an Experimental Model to Study Epigenetic Modifiers of Electrophysiology.Cells · 2022Review
- Transcriptomic Evidence of the Immune Response Activation in Individuals With Limb Girdle Muscular Dystrophy Dominant 2 (LGMDD2) Contributes to Resistance to HIV-1 Infection.Frontiers in cell and developmental biology · 2022Article
- Antiquated ejection fraction: Basic research applications for speckle tracking echocardiography.Frontiers in physiology · 2022Review
- NOX1 promotes myocardial fibrosis and cardiac dysfunctionFrontiers in pharmacology · 2022Article
- C-X-C motif chemokine ligand 12: a potential therapeutic target in Duchenne muscular dystrophy.Bioengineered · 2021Article
- Influence of Different Types of Corticosteroids on Heart Rate Variability of Individuals with Duchenne Muscular Dystrophy-A Pilot Cross Sectional Study.Life (Basel, Switzerland) · 2021Article
- Standard of care versus new-wave corticosteroids in the treatment of Duchenne muscular dystrophy: Can we do better?Orphanet journal of rare diseases · 2021Review
- A Phase 1/2 Study of Flavocoxid, an Oral NF-κB Inhibitor, in Duchenne Muscular Dystrophy.Brain sciences · 2021Article
- Understanding the common mechanisms of heart and skeletal muscle wasting in cancer cachexia.Oncogenesis · 2021Review
Corrections and comments
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Authors and funding
21 authors at 11 institutions in 2 countries.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a neuromuscular disorder causing progressive muscle degeneration. Although cardiomyopathy is a leading mortality cause in DMD patients, the mechanisms underlying heart failure are not well understood. Previously, we showed that NF-κB exacerbates DMD skeletal muscle pathology by promoting inflammation and impairing new muscle growth. Here, we show that NF-κB is activated in murine dystrophic (mdx) hearts, and that cardiomyocyte ablation of NF-κB rescues cardiac function. This physiological improvement is associated with a signature of upregulated calcium genes, coinciding with global enrichment of permissive H3K27 acetylation chromatin marks and depletion of the transcriptional repressors CCCTC-binding factor, SIN3 transcription regulator family member A, and histone deacetylase 1. In this respect, in DMD hearts, NF-κB acts differently from its established role as a transcriptional activator, instead promoting global changes in the chromatin landscape to regulate calcium genes and cardiac function.
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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.