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1
Exosomal miR-223 Contributes to Mesenchymal Stem Cell-Elicited Cardioprotection in Polymicrobial Sepsis
Exosomal miR-223 Contributes to Mesenchymal Stem Cell-Elicited Cardioprotection in Polymicrobial Sepsis
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Exosomal miR-223 Contributes to Mesenchymal Stem Cell-Elicited Cardioprotection in Polymicrobial Sepsis

Scientific reports, 2015-09, Vol.5 (1), p.13721-13721, Article 13721 [Peer Reviewed Journal]

Copyright Nature Publishing Group Sep 2015 ;Copyright © 2015, Macmillan Publishers Limited 2015 Macmillan Publishers Limited ;ISSN: 2045-2322 ;EISSN: 2045-2322 ;DOI: 10.1038/srep13721 ;PMID: 26348153

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2
Loss of β-catenin in resident cardiac fibroblasts attenuates fibrosis induced by pressure overload in mice
Loss of β-catenin in resident cardiac fibroblasts attenuates fibrosis induced by pressure overload in mice
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Loss of β-catenin in resident cardiac fibroblasts attenuates fibrosis induced by pressure overload in mice

Nature communications, 2017-09, Vol.8 (1), p.712-12, Article 712 [Peer Reviewed Journal]

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: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-017-00840-w ;PMID: 28959037

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3
Fibroblast-specific TGF-β-Smad2/3 signaling underlies cardiac fibrosis
Fibroblast-specific TGF-β-Smad2/3 signaling underlies cardiac fibrosis
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Fibroblast-specific TGF-β-Smad2/3 signaling underlies cardiac fibrosis

The Journal of clinical investigation, 2017-10, Vol.127 (10), p.3770-3783 [Peer Reviewed Journal]

Copyright American Society for Clinical Investigation Oct 2017 ;Copyright © 2017, American Society for Clinical Investigation 2017 American Society for Clinical Investigation ;ISSN: 0021-9738 ;EISSN: 1558-8238 ;DOI: 10.1172/JCI94753 ;PMID: 28891814

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4
Genetic Factors Are Not the Major Causes of Chronic Diseases
Genetic Factors Are Not the Major Causes of Chronic Diseases
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Genetic Factors Are Not the Major Causes of Chronic Diseases

PloS one, 2016-04, Vol.11 (4), p.e0154387 [Peer Reviewed Journal]

COPYRIGHT 2016 Public Library of Science ;COPYRIGHT 2016 Public Library of Science ;2016 Stephen M. Rappaport. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2016 Stephen M. Rappaport 2016 Stephen M. Rappaport ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0154387 ;PMID: 27105432

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5
Fatal heart disease among cancer patients
Fatal heart disease among cancer patients
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Fatal heart disease among cancer patients

Nature communications, 2020-04, Vol.11 (1), p.2011-2011, Article 2011 [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/s41467-020-15639-5 ;PMID: 32332714

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6
STING-IRF3 contributes to lipopolysaccharide-induced cardiac dysfunction, inflammation, apoptosis and pyroptosis by activating NLRP3
STING-IRF3 contributes to lipopolysaccharide-induced cardiac dysfunction, inflammation, apoptosis and pyroptosis by activating NLRP3
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STING-IRF3 contributes to lipopolysaccharide-induced cardiac dysfunction, inflammation, apoptosis and pyroptosis by activating NLRP3

Redox biology, 2019-06, Vol.24, p.101215, Article 101215 [Peer Reviewed Journal]

Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved. ;2019 The Authors 2019 ;ISSN: 2213-2317 ;EISSN: 2213-2317 ;DOI: 10.1016/j.redox.2019.101215 ;PMID: 31121492

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7
Radiation-induced heart disease: a review of classification, mechanism and prevention
Radiation-induced heart disease: a review of classification, mechanism and prevention
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Radiation-induced heart disease: a review of classification, mechanism and prevention

International journal of biological sciences, 2019-01, Vol.15 (10), p.2128-2138 [Peer Reviewed Journal]

The author(s). ;Copyright BioMed Central 2019 ;2019. This work is published under https://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: 1449-2288 ;EISSN: 1449-2288 ;DOI: 10.7150/ijbs.35460 ;PMID: 31592122

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8
Elevated circulating high-sensitivity cardiac troponin t and cardiac remodeling in obesity
Elevated circulating high-sensitivity cardiac troponin t and cardiac remodeling in obesity
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Elevated circulating high-sensitivity cardiac troponin t and cardiac remodeling in obesity

BMC cardiovascular disorders, 2021-12, Vol.21 (1), p.620-620, Article 620 [Peer Reviewed Journal]

2021. The Author(s). ;COPYRIGHT 2021 BioMed Central Ltd. ;2021. This work is licensed 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: 1471-2261 ;EISSN: 1471-2261 ;DOI: 10.1186/s12872-021-02445-0 ;PMID: 34963447

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9
Cigarette and e-cigarette dual use and risk of cardiopulmonary symptoms in the Health eHeart Study
Cigarette and e-cigarette dual use and risk of cardiopulmonary symptoms in the Health eHeart Study
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Cigarette and e-cigarette dual use and risk of cardiopulmonary symptoms in the Health eHeart Study

PloS one, 2018-07, Vol.13 (7), p.e0198681 [Peer Reviewed Journal]

COPYRIGHT 2018 Public Library of Science ;COPYRIGHT 2018 Public Library of Science ;2018 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2018 Wang et al 2018 Wang et al ;ISSN: 1932-6203 ;EISSN: 1932-6203 ;DOI: 10.1371/journal.pone.0198681 ;PMID: 30044773

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10
MicroRNAs in Cardiac Diseases
MicroRNAs in Cardiac Diseases
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MicroRNAs in Cardiac Diseases

Cells (Basel, Switzerland), 2019-07, Vol.8 (7), p.737 [Peer Reviewed Journal]

2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2019 by the authors. 2019 ;ISSN: 2073-4409 ;EISSN: 2073-4409 ;DOI: 10.3390/cells8070737 ;PMID: 31323768

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11
Non-invasive detection of human cardiomyocyte death using methylation patterns of circulating DNA
Non-invasive detection of human cardiomyocyte death using methylation patterns of circulating DNA
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Non-invasive detection of human cardiomyocyte death using methylation patterns of circulating DNA

Nature communications, 2018-04, Vol.9 (1), p.1443-9, Article 1443 [Peer Reviewed Journal]

Copyright Nature Publishing Group Apr 2018 ;The Author(s) 2018 ;ISSN: 2041-1723 ;EISSN: 2041-1723 ;DOI: 10.1038/s41467-018-03961-y ;PMID: 29691397

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12
The SGLT-2 inhibitor empagliflozin improves myocardial strain, reduces cardiac fibrosis and pro-inflammatory cytokines in non-diabetic mice treated with doxorubicin
The SGLT-2 inhibitor empagliflozin improves myocardial strain, reduces cardiac fibrosis and pro-inflammatory cytokines in non-diabetic mice treated with doxorubicin
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The SGLT-2 inhibitor empagliflozin improves myocardial strain, reduces cardiac fibrosis and pro-inflammatory cytokines in non-diabetic mice treated with doxorubicin

Cardiovascular diabetology, 2021-07, Vol.20 (1), p.150-20, Article 150 [Peer Reviewed Journal]

2021. The Author(s). ;2021. This work is licensed 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: 1475-2840 ;EISSN: 1475-2840 ;DOI: 10.1186/s12933-021-01346-y ;PMID: 34301253

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13
VEGF-A in Cardiomyocytes and Heart Diseases
VEGF-A in Cardiomyocytes and Heart Diseases
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VEGF-A in Cardiomyocytes and Heart Diseases

International journal of molecular sciences, 2020-07, Vol.21 (15), p.5294 [Peer Reviewed Journal]

2020. This work is licensed under http://creativecommons.org/licenses/by/3.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;2020 by the authors. 2020 ;ISSN: 1422-0067 ;ISSN: 1661-6596 ;EISSN: 1422-0067 ;DOI: 10.3390/ijms21155294 ;PMID: 32722551

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14
European Cardiovascular Magnetic Resonance (EuroCMR) registry--multi national results from 57 centers in 15 countries
European Cardiovascular Magnetic Resonance (EuroCMR) registry--multi national results from 57 centers in 15 countries
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European Cardiovascular Magnetic Resonance (EuroCMR) registry--multi national results from 57 centers in 15 countries

Journal of cardiovascular magnetic resonance, 2013-01, Vol.15 (1), p.9-9, Article 9 [Peer Reviewed Journal]

COPYRIGHT 2013 BioMed Central Ltd. ;COPYRIGHT 2013 BioMed Central Ltd. ;2013 Bruder et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. ;Copyright ©2013 Bruder et al.; licensee BioMed Central Ltd. 2013 Bruder et al.; licensee BioMed Central Ltd. ;ISSN: 1532-429X ;ISSN: 1097-6647 ;EISSN: 1532-429X ;DOI: 10.1186/1532-429x-15-9 ;PMID: 23331632

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15
Natriuretic Peptides in the Regulation of Cardiovascular Physiology and Metabolic Events
Natriuretic Peptides in the Regulation of Cardiovascular Physiology and Metabolic Events
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Natriuretic Peptides in the Regulation of Cardiovascular Physiology and Metabolic Events

Journal of the American Heart Association, 2015-10, Vol.4 (10), p.e002423 [Peer Reviewed Journal]

2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. ;ISSN: 2047-9980 ;EISSN: 2047-9980 ;DOI: 10.1161/jaha.115.002423 ;PMID: 26508744

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16
Canagliflozin attenuates isoprenaline-induced cardiac oxidative stress by stimulating multiple antioxidant and anti-inflammatory signaling pathways
Canagliflozin attenuates isoprenaline-induced cardiac oxidative stress by stimulating multiple antioxidant and anti-inflammatory signaling pathways
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Canagliflozin attenuates isoprenaline-induced cardiac oxidative stress by stimulating multiple antioxidant and anti-inflammatory signaling pathways

Scientific reports, 2020-09, Vol.10 (1), p.14459, Article 14459 [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/s41598-020-71449-1 ;PMID: 32879422

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17
Sirtuin-3 (SIRT3) Protein Attenuates Doxorubicin-induced Oxidative Stress and Improves Mitochondrial Respiration in H9c2 Cardiomyocytes
Sirtuin-3 (SIRT3) Protein Attenuates Doxorubicin-induced Oxidative Stress and Improves Mitochondrial Respiration in H9c2 Cardiomyocytes
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Sirtuin-3 (SIRT3) Protein Attenuates Doxorubicin-induced Oxidative Stress and Improves Mitochondrial Respiration in H9c2 Cardiomyocytes

The Journal of biological chemistry, 2015-04, Vol.290 (17), p.10981-10993 [Peer Reviewed Journal]

2015 © 2015 ASBMB. Currently published by Elsevier Inc; originally published by American Society for Biochemistry and Molecular Biology. ;2015 by The American Society for Biochemistry and Molecular Biology, Inc. ;2015 by The American Society for Biochemistry and Molecular Biology, Inc. 2015 ;ISSN: 0021-9258 ;EISSN: 1083-351X ;DOI: 10.1074/jbc.M114.607960 ;PMID: 25759382

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18
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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19
Changes in Cardiovascular Biomarkers With Breast Cancer Therapy and Associations With Cardiac Dysfunction
Changes in Cardiovascular Biomarkers With Breast Cancer Therapy and Associations With Cardiac Dysfunction
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Changes in Cardiovascular Biomarkers With Breast Cancer Therapy and Associations With Cardiac Dysfunction

Journal of the American Heart Association, 2020-01, Vol.9 (2), p.e014708 [Peer Reviewed Journal]

2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. ;ISSN: 2047-9980 ;EISSN: 2047-9980 ;DOI: 10.1161/JAHA.119.014708 ;PMID: 31959034

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20
CaMKII Activity in the Inflammatory Response of Cardiac Diseases
CaMKII Activity in the Inflammatory Response of Cardiac Diseases
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CaMKII Activity in the Inflammatory Response of Cardiac Diseases

International journal of molecular sciences, 2019-09, Vol.20 (18), p.4374 [Peer Reviewed Journal]

2019. This work is licensed under https://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. ;2019 by the authors. 2019 ;ISSN: 1422-0067 ;ISSN: 1661-6596 ;EISSN: 1422-0067 ;DOI: 10.3390/ijms20184374 ;PMID: 31489895

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