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1
Prevention of exercised induced cardiomyopathy following Pip-PMO treatment in dystrophic mdx mice
Prevention of exercised induced cardiomyopathy following Pip-PMO treatment in dystrophic mdx mice
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Prevention of exercised induced cardiomyopathy following Pip-PMO treatment in dystrophic mdx mice

Scientific reports, 2015-03, Vol.5 (1), p.8986-8986, Article 8986 [Peer Reviewed Journal]

Copyright Nature Publishing Group Mar 2015 ;Copyright © 2015, Macmillan Publishers Limited. All rights reserved 2015 Macmillan Publishers Limited. All rights reserved ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/srep08986 ;PMID: 25758104

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2
Genetic basis of cardiomyopathy and the genotypes involved in prognosis and left ventricular reverse remodeling
Genetic basis of cardiomyopathy and the genotypes involved in prognosis and left ventricular reverse remodeling
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Genetic basis of cardiomyopathy and the genotypes involved in prognosis and left ventricular reverse remodeling

Scientific reports, 2018-01, Vol.8 (1), p.1998-11, Article 1998 [Peer Reviewed Journal]

2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2018 ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/s41598-018-20114-9 ;PMID: 29386531

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3
Silencing long non-coding RNA Kcnq1ot1 alleviates pyroptosis and fibrosis in diabetic cardiomyopathy
Silencing long non-coding RNA Kcnq1ot1 alleviates pyroptosis and fibrosis in diabetic cardiomyopathy
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Silencing long non-coding RNA Kcnq1ot1 alleviates pyroptosis and fibrosis in diabetic cardiomyopathy

Cell death & disease, 2018-09, Vol.9 (10), p.1000-13, Article 1000 [Peer Reviewed Journal]

2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2018 ;ISSN: 2041-4889 ;EISSN: 2041-4889 ;DOI: 10.1038/s41419-018-1029-4 ;PMID: 30250027

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4
Analysis of cardiac magnetic resonance imaging in 36,000 individuals yields genetic insights into dilated cardiomyopathy
Analysis of cardiac magnetic resonance imaging in 36,000 individuals yields genetic insights into dilated cardiomyopathy
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Analysis of cardiac magnetic resonance imaging in 36,000 individuals yields genetic insights into dilated cardiomyopathy

Nature communications, 2020-05, Vol.11 (1), p.2254-2254, Article 2254 [Peer Reviewed Journal]

The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2020 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-020-15823-7 ;PMID: 32382064

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5
WWP2 regulates pathological cardiac fibrosis by modulating SMAD2 signaling
WWP2 regulates pathological cardiac fibrosis by modulating SMAD2 signaling
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WWP2 regulates pathological cardiac fibrosis by modulating SMAD2 signaling

Nature communications, 2019-08, Vol.10 (1), p.3616-19, Article 3616 [Peer Reviewed Journal]

2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;Attribution ;The Author(s) 2019 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-019-11551-9 ;PMID: 31399586

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6
Striated muscle-specific base editing enables correction of mutations causing dilated cardiomyopathy
Striated muscle-specific base editing enables correction of mutations causing dilated cardiomyopathy
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Striated muscle-specific base editing enables correction of mutations causing dilated cardiomyopathy

Nature communications, 2023-06, Vol.14 (1), p.3714-3714, Article 3714 [Peer Reviewed Journal]

2023. The Author(s). ;The Author(s) 2023. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2023 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-023-39352-1 ;PMID: 37349314

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7
Homogeneous 2D and 3D alignment of cardiomyocyte in dilated cardiomyopathy revealed by intravital heart imaging
Homogeneous 2D and 3D alignment of cardiomyocyte in dilated cardiomyopathy revealed by intravital heart imaging
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Homogeneous 2D and 3D alignment of cardiomyocyte in dilated cardiomyopathy revealed by intravital heart imaging

Scientific reports, 2021-07, Vol.11 (1), p.14698-14698, Article 14698 [Peer Reviewed Journal]

2021. The Author(s). ;The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2021 ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/s41598-021-94100-z ;PMID: 34282197

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8
Investigation of diets associated with dilated cardiomyopathy in dogs using foodomics analysis
Investigation of diets associated with dilated cardiomyopathy in dogs using foodomics analysis
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Investigation of diets associated with dilated cardiomyopathy in dogs using foodomics analysis

Scientific reports, 2021-08, Vol.11 (1), p.15881-12, Article 15881 [Peer Reviewed Journal]

2021. The Author(s). ;The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2021 ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/s41598-021-94464-2 ;PMID: 34354102

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9
Intergenerational inheritance of high fat diet-induced cardiac lipotoxicity in Drosophila
Intergenerational inheritance of high fat diet-induced cardiac lipotoxicity in Drosophila
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Intergenerational inheritance of high fat diet-induced cardiac lipotoxicity in Drosophila

Nature communications, 2019-01, Vol.10 (1), p.193-14, Article 193 [Peer Reviewed Journal]

This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2019 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-018-08128-3 ;PMID: 30643137

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10
High glucose induces Drp1-mediated mitochondrial fission via the Orai1 calcium channel to participate in diabetic cardiomyocyte hypertrophy
High glucose induces Drp1-mediated mitochondrial fission via the Orai1 calcium channel to participate in diabetic cardiomyocyte hypertrophy
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High glucose induces Drp1-mediated mitochondrial fission via the Orai1 calcium channel to participate in diabetic cardiomyocyte hypertrophy

Cell death & disease, 2021-02, Vol.12 (2), p.216-216, Article 216 [Peer Reviewed Journal]

The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2021 ;ISSN: 2041-4889 ;EISSN: 2041-4889 ;DOI: 10.1038/s41419-021-03502-4 ;PMID: 33637715

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11
Phospholamban antisense oligonucleotides improve cardiac function in murine cardiomyopathy
Phospholamban antisense oligonucleotides improve cardiac function in murine cardiomyopathy
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Phospholamban antisense oligonucleotides improve cardiac function in murine cardiomyopathy

Nature communications, 2021-08, Vol.12 (1), p.5180-5180, Article 5180 [Peer Reviewed Journal]

2021. The Author(s). ;The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2021 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-021-25439-0 ;PMID: 34462437

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12
Gain-of-function cardiomyopathic mutations in RBM20 rewire splicing regulation and re-distribute ribonucleoprotein granules within processing bodies
Gain-of-function cardiomyopathic mutations in RBM20 rewire splicing regulation and re-distribute ribonucleoprotein granules within processing bodies
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Gain-of-function cardiomyopathic mutations in RBM20 rewire splicing regulation and re-distribute ribonucleoprotein granules within processing bodies

Nature communications, 2021-11, Vol.12 (1), p.6324-6324, Article 6324 [Peer Reviewed Journal]

2021. The Author(s). ;The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2021 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-021-26623-y ;PMID: 34732726

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13
Correction of human phospholamban R14del mutation associated with cardiomyopathy using targeted nucleases and combination therapy
Correction of human phospholamban R14del mutation associated with cardiomyopathy using targeted nucleases and combination therapy
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Correction of human phospholamban R14del mutation associated with cardiomyopathy using targeted nucleases and combination therapy

Nature communications, 2015-04, Vol.6 (1), p.6955, Article 6955 [Peer Reviewed Journal]

Copyright Nature Publishing Group Apr 2015 ;Attribution ;Copyright © 2015, Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2015 Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/ncomms7955 ;PMID: 25923014

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14
The K219T-Lamin mutation induces conduction defects through epigenetic inhibition of SCN5A in human cardiac laminopathy
The K219T-Lamin mutation induces conduction defects through epigenetic inhibition of SCN5A in human cardiac laminopathy
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The K219T-Lamin mutation induces conduction defects through epigenetic inhibition of SCN5A in human cardiac laminopathy

Nature communications, 2019-05, Vol.10 (1), p.2267-2267, Article 2267 [Peer Reviewed Journal]

The Author(s) 2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2019 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-019-09929-w ;PMID: 31118417

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15
Circulating microRNA signature for the diagnosis of childhood dilated cardiomyopathy
Circulating microRNA signature for the diagnosis of childhood dilated cardiomyopathy
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Circulating microRNA signature for the diagnosis of childhood dilated cardiomyopathy

Scientific reports, 2018-01, Vol.8 (1), p.724-9, Article 724 [Peer Reviewed Journal]

2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2018 ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/s41598-017-19138-4 ;PMID: 29335596

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16
Serum circular RNAs act as blood-based biomarkers for hypertrophic obstructive cardiomyopathy
Serum circular RNAs act as blood-based biomarkers for hypertrophic obstructive cardiomyopathy
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Serum circular RNAs act as blood-based biomarkers for hypertrophic obstructive cardiomyopathy

Scientific reports, 2019-12, Vol.9 (1), p.20350-8, Article 20350 [Peer Reviewed Journal]

2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2019 ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/s41598-019-56617-2 ;PMID: 31889077

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17
Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes
Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes
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Abnormal contractility in human heart myofibrils from patients with dilated cardiomyopathy due to mutations in TTN and contractile protein genes

Scientific reports, 2017-11, Vol.7 (1), p.14829-11, Article 14829 [Peer Reviewed Journal]

Scientific Reports is a copyright of Springer, 2017. ;2017. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2017 ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/s41598-017-13675-8 ;PMID: 29093449

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18
Mechanistic clues to the protective effect of chrysin against doxorubicin-induced cardiomyopathy: Plausible roles of p53, MAPK and AKT pathways
Mechanistic clues to the protective effect of chrysin against doxorubicin-induced cardiomyopathy: Plausible roles of p53, MAPK and AKT pathways
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Mechanistic clues to the protective effect of chrysin against doxorubicin-induced cardiomyopathy: Plausible roles of p53, MAPK and AKT pathways

Scientific reports, 2017-07, Vol.7 (1), p.4795-13, Article 4795 [Peer Reviewed Journal]

Copyright Nature Publishing Group Jul 2017 ;The Author(s) 2017 ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/s41598-017-05005-9 ;PMID: 28684738

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19
Prevalence, functional characteristics, and clinical significance of right ventricular involvement in patients with hypertrophic cardiomyopathy
Prevalence, functional characteristics, and clinical significance of right ventricular involvement in patients with hypertrophic cardiomyopathy
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Prevalence, functional characteristics, and clinical significance of right ventricular involvement in patients with hypertrophic cardiomyopathy

Scientific reports, 2020-12, Vol.10 (1), p.21908-21908, Article 21908 [Peer Reviewed Journal]

The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2020 ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/s41598-020-78945-4 ;PMID: 33318610

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20
lncRNA MIAT functions as a competing endogenous RNA to upregulate DAPK2 by sponging miR-22-3p in diabetic cardiomyopathy
lncRNA MIAT functions as a competing endogenous RNA to upregulate DAPK2 by sponging miR-22-3p in diabetic cardiomyopathy
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lncRNA MIAT functions as a competing endogenous RNA to upregulate DAPK2 by sponging miR-22-3p in diabetic cardiomyopathy

Cell death & disease, 2017-07, Vol.8 (7), p.e2929-e2929 [Peer Reviewed Journal]

Copyright Nature Publishing Group Jul 2017 ;Copyright © 2017 The Author(s) 2017 The Author(s) ;ISSN: 2041-4889 ;EISSN: 2041-4889 ;DOI: 10.1038/cddis.2017.321 ;PMID: 28703801

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