ArticleCirculation research2017
Distinct Cellular Basis for Early Cardiac Arrhythmias, the Cardinal Manifestation of Arrhythmogenic Cardiomyopathy, and the Skin Phenotype of Cardiocutaneous Syndromes.
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Article in Circulation research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16citing papers in PubMed
3.2field-weighted citation impact, top 7% of its field
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Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Protein glycosylation in cardiovascular health and disease.Nature reviews. Cardiology · 2024Review
- PANoptosis is a prominent feature of desmoplakin cardiomyopathy.The journal of cardiovascular aging · 2023Article
- From diagnostic testing to precision medicine: the evolving role of genomics in cardiac channelopathies and cardiomyopathies in children.Current opinion in genetics & development · 2022Review
- Towards a Better Understanding of Genotype-Phenotype Correlations and Therapeutic Targets for Cardiocutaneous Genes: The Importance of Functional Studies above Prediction.International journal of molecular sciences · 2022Review
- Cytoskeletal Protein Variants Driving Atrial Fibrillation: Potential Mechanisms of Action.Cells · 2022Review
- The WNT/β-catenin pathway regulates expression of the genes involved in cell cycle progression and mitochondrial oxidative phosphorylation in the postmitotic cardiac myocytes.The journal of cardiovascular aging · 2022Article
- Haploinsufficiency of Tmem43 in cardiac myocytes activates the DNA damage response pathway leading to a late-onset senescence-associated pro-fibrotic cardiomyopathy.Cardiovascular research · 2021Article
- Single-Cell RNA Sequencing Uncovers Paracrine Functions of the Epicardial-Derived Cells in Arrhythmogenic Cardiomyopathy.Circulation · 2021Article
- Cardiomyocyte adhesion and hyperadhesion differentially require ERK1/2 and plakoglobin.JCI insight · 2020Article
- BET bromodomain inhibition attenuates cardiac phenotype in myocyte-specific lamin A/C-deficient mice.The Journal of clinical investigation · 2020Article
- Genetic basis and molecular biology of cardiac arrhythmias in cardiomyopathies.Cardiovascular research · 2020Review
- Exercise restores dysregulated gene expression in a mouse model of arrhythmogenic cardiomyopathy.Cardiovascular research · 2020Article
- Molecular mechanisms of arrhythmogenic cardiomyopathy.Nature reviews. Cardiology · 2019Review
- Genomic Reorganization of Lamin-Associated Domains in Cardiac Myocytes Is Associated With Differential Gene Expression and DNA Methylation in Human Dilated Cardiomyopathy.Circulation research · 2019Article
- DNA Damage Response/TP53 Pathway Is Activated and Contributes to the Pathogenesis of Dilated Cardiomyopathy Associated With LMNA (Lamin A/C) Mutations.Circulation research · 2019Article
- Suppression of Activated FOXO Transcription Factors in the Heart Prolongs Survival in a Mouse Model of Laminopathies.Circulation research · 2018Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Jennifer KarmouchFrom the Center for Cardiovascular Genetics, Institute of Molecular Medicine, The University of Texas Health Sciences Center, Houston (J.K., Q.Q.Z., R.L., J.T.W., A.J.M.); Texas Heart Institute, Houston (J.T.W., A.J.M.); Cardiovascular Research Institute, Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX (C.Y.M., X.H.T.W.); Department of Pediatrics, Texas Children Hospital, Houston (C.Y.M.); Hubrecht Institute, University Medical Center, Utrecht, The Netherlands (K.K., M.B.-H., H.C.); Royal Netherlands Academy of Arts and Sciences and Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands (H.C.); and École Normale Supérieure de Lyon, France (M.B.-H.).
Qiong Q ZhouFrom the Center for Cardiovascular Genetics, Institute of Molecular Medicine, The University of Texas Health Sciences Center, Houston (J.K., Q.Q.Z., R.L., J.T.W., A.J.M.); Texas Heart Institute, Houston (J.T.W., A.J.M.); Cardiovascular Research Institute, Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX (C.Y.M., X.H.T.W.); Department of Pediatrics, Texas Children Hospital, Houston (C.Y.M.); Hubrecht Institute, University Medical Center, Utrecht, The Netherlands (K.K., M.B.-H., H.C.); Royal Netherlands Academy of Arts and Sciences and Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands (H.C.); and École Normale Supérieure de Lyon, France (M.B.-H.).
Christina Y MiyakeFrom the Center for Cardiovascular Genetics, Institute of Molecular Medicine, The University of Texas Health Sciences Center, Houston (J.K., Q.Q.Z., R.L., J.T.W., A.J.M.); Texas Heart Institute, Houston (J.T.W., A.J.M.); Cardiovascular Research Institute, Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX (C.Y.M., X.H.T.W.); Department of Pediatrics, Texas Children Hospital, Houston (C.Y.M.); Hubrecht Institute, University Medical Center, Utrecht, The Netherlands (K.K., M.B.-H., H.C.); Royal Netherlands Academy of Arts and Sciences and Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands (H.C.); and École Normale Supérieure de Lyon, France (M.B.-H.).
Raffaella LombardiFrom the Center for Cardiovascular Genetics, Institute of Molecular Medicine, The University of Texas Health Sciences Center, Houston (J.K., Q.Q.Z., R.L., J.T.W., A.J.M.); Texas Heart Institute, Houston (J.T.W., A.J.M.); Cardiovascular Research Institute, Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX (C.Y.M., X.H.T.W.); Department of Pediatrics, Texas Children Hospital, Houston (C.Y.M.); Hubrecht Institute, University Medical Center, Utrecht, The Netherlands (K.K., M.B.-H., H.C.); Royal Netherlands Academy of Arts and Sciences and Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands (H.C.); and École Normale Supérieure de Lyon, France (M.B.-H.).
Kai KretzschmarFrom the Center for Cardiovascular Genetics, Institute of Molecular Medicine, The University of Texas Health Sciences Center, Houston (J.K., Q.Q.Z., R.L., J.T.W., A.J.M.); Texas Heart Institute, Houston (J.T.W., A.J.M.); Cardiovascular Research Institute, Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX (C.Y.M., X.H.T.W.); Department of Pediatrics, Texas Children Hospital, Houston (C.Y.M.); Hubrecht Institute, University Medical Center, Utrecht, The Netherlands (K.K., M.B.-H., H.C.); Royal Netherlands Academy of Arts and Sciences and Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands (H.C.); and École Normale Supérieure de Lyon, France (M.B.-H.).
Marie Bannier-HélaouëtFrom the Center for Cardiovascular Genetics, Institute of Molecular Medicine, The University of Texas Health Sciences Center, Houston (J.K., Q.Q.Z., R.L., J.T.W., A.J.M.); Texas Heart Institute, Houston (J.T.W., A.J.M.); Cardiovascular Research Institute, Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX (C.Y.M., X.H.T.W.); Department of Pediatrics, Texas Children Hospital, Houston (C.Y.M.); Hubrecht Institute, University Medical Center, Utrecht, The Netherlands (K.K., M.B.-H., H.C.); Royal Netherlands Academy of Arts and Sciences and Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands (H.C.); and École Normale Supérieure de Lyon, France (M.B.-H.).
Hans CleversFrom the Center for Cardiovascular Genetics, Institute of Molecular Medicine, The University of Texas Health Sciences Center, Houston (J.K., Q.Q.Z., R.L., J.T.W., A.J.M.); Texas Heart Institute, Houston (J.T.W., A.J.M.); Cardiovascular Research Institute, Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX (C.Y.M., X.H.T.W.); Department of Pediatrics, Texas Children Hospital, Houston (C.Y.M.); Hubrecht Institute, University Medical Center, Utrecht, The Netherlands (K.K., M.B.-H., H.C.); Royal Netherlands Academy of Arts and Sciences and Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands (H.C.); and École Normale Supérieure de Lyon, France (M.B.-H.).
Xander H T WehrensFrom the Center for Cardiovascular Genetics, Institute of Molecular Medicine, The University of Texas Health Sciences Center, Houston (J.K., Q.Q.Z., R.L., J.T.W., A.J.M.); Texas Heart Institute, Houston (J.T.W., A.J.M.); Cardiovascular Research Institute, Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX (C.Y.M., X.H.T.W.); Department of Pediatrics, Texas Children Hospital, Houston (C.Y.M.); Hubrecht Institute, University Medical Center, Utrecht, The Netherlands (K.K., M.B.-H., H.C.); Royal Netherlands Academy of Arts and Sciences and Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands (H.C.); and École Normale Supérieure de Lyon, France (M.B.-H.).
James T WillersonFrom the Center for Cardiovascular Genetics, Institute of Molecular Medicine, The University of Texas Health Sciences Center, Houston (J.K., Q.Q.Z., R.L., J.T.W., A.J.M.); Texas Heart Institute, Houston (J.T.W., A.J.M.); Cardiovascular Research Institute, Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX (C.Y.M., X.H.T.W.); Department of Pediatrics, Texas Children Hospital, Houston (C.Y.M.); Hubrecht Institute, University Medical Center, Utrecht, The Netherlands (K.K., M.B.-H., H.C.); Royal Netherlands Academy of Arts and Sciences and Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands (H.C.); and École Normale Supérieure de Lyon, France (M.B.-H.).
Ali J MarianFrom the Center for Cardiovascular Genetics, Institute of Molecular Medicine, The University of Texas Health Sciences Center, Houston (J.K., Q.Q.Z., R.L., J.T.W., A.J.M.); Texas Heart Institute, Houston (J.T.W., A.J.M.); Cardiovascular Research Institute, Department of Molecular Physiology and Biophysics, Baylor College of Medicine, Houston, TX (C.Y.M., X.H.T.W.); Department of Pediatrics, Texas Children Hospital, Houston (C.Y.M.); Hubrecht Institute, University Medical Center, Utrecht, The Netherlands (K.K., M.B.-H., H.C.); Royal Netherlands Academy of Arts and Sciences and Princess Máxima Center for Pediatric Oncology, Utrecht, The Netherlands (H.C.); and École Normale Supérieure de Lyon, France (M.B.-H.). ali.j.marian@uth.tmc.edu.
Texas Children's Hospital · USHubrecht Institute for Developmental Biology and Stem Cell Research · NLHouston Methodist · USUniversity Medical Center Utrecht · NL
Funding
Ryanodine receptor regulation in post-operative atrial fibrillationR01HL089598 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2007 to 2022
$6.5MPathogenic Role of Selected Cardiac Myocyte- and Fibroblast-Specific Epigenetic Changes in LaminopathiesR01HL132401 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI Ali J Marian · 2016 to 2026
$6.0MCanonical Wnt Signaling in Pathogenesis and Rescue of ARVC PhenotypeR01HL088498 · NHLBI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MARIAN, ALI J · 2008 to 2017
$3.4MRegulation of Sarcoplasmic Reticulum Calcium Release in Heart FailureR01HL091947 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2009 to 2019
$3.2MDetermining the Role of Junctophilin-2 in Cardiac DiseaseR01HL117641 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI WEHRENS, XANDER H.T. · 2014 to 2017
$2.3MDevelopment of novel compounds for the treatment of atrial fibrillationR41HL129570 · NHLBI · ELEX BIOTECH, LLC · PI WEHRENS, XANDER H.T. · 2015 to 2015
$428kCardiovascular Ultrasonography UnitS10OD018135 · OD · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MARIAN, ALI J · 2015 to 2015
$184kNHLBI NIH HHS R01 HL088498NHLBI NIH HHS R01 HL089598NHLBI NIH HHS R01 HL091947NHLBI NIH HHS R01 HL117641NHLBI NIH HHS R01 HL132401NHLBI NIH HHS R41 HL129570NIH HHS S10 OD018135
Abstract
rationaleArrhythmogenic cardiomyopathy is caused primarily by mutations in genes encoding desmosome proteins. Ventricular arrhythmias are the cardinal and typically early manifestations, whereas myocardial fibroadiposis is the pathological hallmark. Homozygous
objectiveTo determine phenotypic consequences of deletion of METHODS AND
resultsExpression of CSPG4 (chondroitin sulfate proteoglycan 4) was detected in epidermal keratinocytes and the cardiac conduction system. CSPG4
conclusionsDeletion of
Indexed as
PhenotypeAnimalsAntigensArrhythmogenic Right Ventricular DysplasiaCells, CulturedChondroitin Sulfate Proteoglycan 4DesmoplakinsHumansKeratinocytesKeratosisMiceMutationMyocytes, CardiacProteoglycansSyndromeAntigensChondroitin Sulfate Proteoglycan 4DesmoplakinsProteoglycansarrhythmogenic right ventricular dysplasiadeath, suddendesmoplakinsdesmosomesneuroglia
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