ArticleHuman molecular genetics2016
ERK1/2 directly acts on CTGF/CCN2 expression to mediate myocardial fibrosis in cardiomyopathy caused by mutations in the lamin A/C gene.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 104 citations in OpenAlex.
- Simtuzumab Attenuates Loxl2-Mediated Extracellular Matrix Remodeling and Preserves Cardiac Function inCirculation. Heart failure · 2026Article
- Dysregulated TGFβ-ERK Signaling Drives Aberrant Extracellular Matrix Production in Noonan Syndrome-Associated Pulmonary Valve Stenosis.bioRxiv : the preprint server for biology · 2026Article
- Deregulated nutrient response in ttntv cardiomyopathy can be repaired via Erk inhibition for cardioprotective effects.Journal of molecular and cellular cardiology · 2025Article
- Profibrotic Molecules Are Reduced in CRISPR-Edited Emery-Dreifuss Muscular Dystrophy Fibroblasts.Cells · 2025Article
- Salt sensitivity and myocardial fibrosis: unraveling the silent cardiovascular remodeling.Frontiers in pharmacology · 2025Review
- Mechanism and research progress of MAPK signaling pathway in myocardial fibrosis.Frontiers in cardiovascular medicine · 2025Review
- Design and screening of novel 1,2,4-Triazole-3-thione derivatives as DCN1 inhibitors for anticardiac fibrosis based on 3D-QSAR modeling and molecular dynamics.Frontiers in pharmacology · 2025Article
- Review
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- Risk Assessment and Personalized Treatment Options in Inherited Dilated Cardiomyopathies: A Narrative Review.Biomedicines · 2024Review
- mTOR Inhibition Prolongs Survival and Has Beneficial Effects on Heart Function After Onset of Lamin A/C Gene Mutation Cardiomyopathy in Mice.Circulation. Heart failure · 2024Article
- From gene to mechanics: a comprehensive insight into the mechanobiology of LMNA mutations in cardiomyopathy.Cell communication and signaling : CCS · 2024Review
- Emerin deficiency does not exacerbate cardiomyopathy in a murine model of Emery-Dreifuss muscular dystrophy caused by an LMNA gene mutation.The journal of physiological sciences : JPS · 2023Article
- LncRNA CFRL aggravates cardiac fibrosis by modulating both miR-3113-5p/CTGF and miR-3473d/FN1 axis.iScience · 2023Article
- Mesenchymal stem cells alleviate dexamethasone-induced muscle atrophy in mice and the involvement of ERK1/2 signalling pathway.Stem cell research & therapy · 2023Article
- Molecular Mechanisms and Risk Factors Related to the Pathogenesis of Peyronie's Disease.International journal of molecular sciences · 2023Review
- Epigenetics inCells · 2023Review
- Comprehensive review on gene mutations contributing to dilated cardiomyopathy.Frontiers in cardiovascular medicine · 2023Review
- Pamrevlumab, a Fully Human Monoclonal Antibody Targeting Connective Tissue Growth Factor, for Non-Ambulatory Patients with Duchenne Muscular Dystrophy.Journal of neuromuscular diseases · 2023Article
- Actin-microtubule cytoskeletal interplay mediated by MRTF-A/SRF signaling promotes dilated cardiomyopathy caused by LMNA mutations.Nature communications · 2022Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 6 institutions in 2 countries.
Funding
Abstract
Cardiomyopathy caused by lamin A/C gene mutations (LMNA cardiomyopathy) is characterized by increased myocardial fibrosis, which impairs left ventricular relaxation and predisposes to heart failure, and cardiac conduction abnormalities. While we previously discovered abnormally elevated extracellular signal-regulated kinase 1/2 (ERK1/2) activities in heart in LMNA cardiomyopathy, its role on the development of myocardial fibrosis remains unclear. We now showed that transforming growth factor (TGF)-β/Smad signaling participates in the activation of ERK1/2 signaling in LMNA cardiomyopathy. ERK1/2 acts on connective tissue growth factor (CTGF/CCN2) expression to mediate the myocardial fibrosis and left ventricular dysfunction. Studies in vivo demonstrate that inhibiting CTGF/CCN2 using a specific antibody decreases myocardial fibrosis and improves the left ventricular dysfunction. Together, these findings show that cardiac ERK1/2 activity is modulated in part by TGF-β/Smad signaling, leading to altered activation of CTGF/CCN2 to mediate fibrosis and alter cardiac function. This identifies a novel mechanism in the development of LMNA cardiomyopathy.
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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.