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Steven P Jones

Showing results (91-100 of 105) with videos related to

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American Journal of Physiology. Cell Physiology|January 28, 2025
Activated cardiac fibroblasts are a primary source of high-molecular-weight hyaluronan productionDanielle T Little, Caitlin M Howard, Emma Pendergraft, et al.
Basic Research in Cardiology|June 2, 2019
E2f1 deletion attenuates infarct-induced ventricular remodeling without affecting O-GlcNAcylationSujith Dassanayaka, Kenneth R Brittian, Andrea Jurkovic, et al.
American Journal of Physiology. Heart and Circulatory Physiology|May 23, 2020
Cardiac mesenchymal cells from failing and nonfailing hearts limit ventricular dilation when administered late after infarctionTimothy N Audam, Yibing Nong, Alex Tomlin, et al.
Circulation|September 2, 2017
Exercise-Induced Changes in Glucose Metabolism Promote Physiological Cardiac GrowthAndrew A Gibb, Paul N Epstein, Shizuka Uchida, et al.
Basic Research in Cardiology|March 17, 2017
Cardiomyocyte Ogt limits ventricular dysfunction in mice following pressure overload without affecting hypertrophySujith Dassanayaka, Robert E Brainard, Lewis J Watson, et al.
Plos One|November 30, 2020
Cardiomyocyte Oga haploinsufficiency increases O-GlcNAcylation but hastens ventricular dysfunction following myocardial infarctionSujith Dassanayaka, Kenneth R Brittian, Bethany W Long, et al.
Circulation. Heart Failure|April 26, 2014
Metabolomic analysis of pressure-overloaded and infarcted mouse heartsBrian E Sansbury, Angelica M DeMartino, Zhengzhi Xie, et al.
American Journal of Physiology. Heart and Circulatory Physiology|September 17, 2021
Cardiac PANK1 deletion exacerbates ventricular dysfunction during pressure overloadTimothy N Audam, Caitlin M Howard, Lauren F Garrett, et al.
Nature Communications|May 26, 2026
TAK1 drives inflammatory fibroblast acquisition and shapes myocardial infarction responses in male miceDaniel C Nguyen, Jonah K Stephan, Lianay Gutierrez Luque, et al.
Circulation Research|December 16, 2014
The NHLBI-sponsored Consortium for preclinicAl assESsment of cARdioprotective therapies (CAESAR): a new paradigm for rigorous, accurate, and reproducible evaluation of putative infarct-sparing interventions in mice, rabbits, and pigsSteven P Jones, Xian-Liang Tang, Yiru Guo, et al.
Pageof 11

Showing results (91-100 of 105) with videos related to

Sort By:
Pageof 11
American Journal of Physiology. Cell Physiology|January 28, 2025
Activated cardiac fibroblasts are a primary source of high-molecular-weight hyaluronan productionDanielle T Little, Caitlin M Howard, Emma Pendergraft, et al.
Basic Research in Cardiology|June 2, 2019
E2f1 deletion attenuates infarct-induced ventricular remodeling without affecting O-GlcNAcylationSujith Dassanayaka, Kenneth R Brittian, Andrea Jurkovic, et al.
American Journal of Physiology. Heart and Circulatory Physiology|May 23, 2020
Cardiac mesenchymal cells from failing and nonfailing hearts limit ventricular dilation when administered late after infarctionTimothy N Audam, Yibing Nong, Alex Tomlin, et al.
Circulation|September 2, 2017
Exercise-Induced Changes in Glucose Metabolism Promote Physiological Cardiac GrowthAndrew A Gibb, Paul N Epstein, Shizuka Uchida, et al.
Basic Research in Cardiology|March 17, 2017
Cardiomyocyte Ogt limits ventricular dysfunction in mice following pressure overload without affecting hypertrophySujith Dassanayaka, Robert E Brainard, Lewis J Watson, et al.
Plos One|November 30, 2020
Cardiomyocyte Oga haploinsufficiency increases O-GlcNAcylation but hastens ventricular dysfunction following myocardial infarctionSujith Dassanayaka, Kenneth R Brittian, Bethany W Long, et al.
Circulation. Heart Failure|April 26, 2014
Metabolomic analysis of pressure-overloaded and infarcted mouse heartsBrian E Sansbury, Angelica M DeMartino, Zhengzhi Xie, et al.
American Journal of Physiology. Heart and Circulatory Physiology|September 17, 2021
Cardiac PANK1 deletion exacerbates ventricular dysfunction during pressure overloadTimothy N Audam, Caitlin M Howard, Lauren F Garrett, et al.
Nature Communications|May 26, 2026
TAK1 drives inflammatory fibroblast acquisition and shapes myocardial infarction responses in male miceDaniel C Nguyen, Jonah K Stephan, Lianay Gutierrez Luque, et al.
Circulation Research|December 16, 2014
The NHLBI-sponsored Consortium for preclinicAl assESsment of cARdioprotective therapies (CAESAR): a new paradigm for rigorous, accurate, and reproducible evaluation of putative infarct-sparing interventions in mice, rabbits, and pigsSteven P Jones, Xian-Liang Tang, Yiru Guo, et al.
Pageof 11