C
Conrad P. Hodgkinson
Researcher at Duke University
Publications - 60
Citations - 2068
Conrad P. Hodgkinson is an academic researcher from Duke University. The author has contributed to research in topics: Reprogramming & Stem cell. The author has an hindex of 24, co-authored 52 publications receiving 1753 citations. Previous affiliations of Conrad P. Hodgkinson include Queen Mary University of London & University of Southampton.
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Journal ArticleDOI
Emerging Concepts in Paracrine Mechanisms in Regenerative Cardiovascular Medicine and Biology
TL;DR: The data suggest the existence of a tissue microenvironment where stem cell factors influence cell survival, inflammation, angiogenesis, repair, and regeneration in a temporal and spatial manner.
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MicroRNA Induced Cardiac Reprogramming In Vivo Evidence for Mature Cardiac Myocytes and Improved Cardiac Function
Tilanthi M. Jayawardena,Elizabeth A. Finch,Lunan Zhang,Hengtao Zhang,Conrad P. Hodgkinson,Richard E. Pratt,Paul B. Rosenberg,Maria Mirotsou,Victor J. Dzau +8 more
TL;DR: There was a time delayed and progressive improvement in fractional shortening and other measures of ventricular function, indicating that miR combo promotes functional recovery of damaged myocardium.
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A Role of Matrix Metalloproteinase-8 in Atherosclerosis
Ross C. Laxton,Yanhua Hu,Johan Duchene,Feng Zhang,Zhongyi Zhang,Kit-Yi Leung,Qingzhong Xiao,Ramona S. Scotland,Conrad P. Hodgkinson,Katherine Smith,Johann Willeit,Carlos López-Otín,Iain A. Simpson,Stefan Kiechl,Amrita Ahluwalia,Qingbo Xu,Shu Ye +16 more
TL;DR: It is found that products of Ang I cleavage by MMP8 increased vascular cell adhesion molecule (VCAM)-1 expression and that M MP8-deficient mice had reduced VCAM-1 expression in atherosclerotic lesions.
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Genetic Engineering of Mesenchymal Stem Cells and Its Application in Human Disease Therapy
TL;DR: The current understanding of the use of genetically engineered mesenchymal stem cells in human disease therapy with emphasis on genetic modifications aimed to improve survival, homing, angiogenesis, and heart function after myocardial infarction is presented.
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Advanced Glycation End-Product of Low Density Lipoprotein Activates the Toll-Like 4 Receptor Pathway Implications for Diabetic Atherosclerosis
TL;DR: Results indicate that AGE-LDL activates a TLR4-mediated signaling pathway, thus inducing proinflammatory cytokine production, which may partly explain the increased risk of atherosclerosis observed in diabetics.