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Sang Mo Kwon

Researcher at Pusan National University

Publications -  21
Citations -  873

Sang Mo Kwon is an academic researcher from Pusan National University. The author has contributed to research in topics: Progenitor cell & Stem cell. The author has an hindex of 15, co-authored 21 publications receiving 741 citations. Previous affiliations of Sang Mo Kwon include Osaka Medical College & New York University.

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Angiogenesis and Its Therapeutic Opportunities

TL;DR: The clinical implications of angiogenesis are reviewed and pro- and antiangiogenic agents that offer potential therapy for cancer and other angiogenic diseases are discussed.
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Tumor necrosis factor-α-activated mesenchymal stem cells promote endothelial progenitor cell homing and angiogenesis.

TL;DR: It is suggested that TNF-α CM stimulates angiogenesis and tissue repair through an increase in homing of EPCs through paracrine mechanisms involving IL-6 and IL-8.
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WKYMVm-induced activation of formyl peptide receptor 2 stimulates ischemic neovasculogenesis by promoting homing of endothelial colony-forming cells

TL;DR: Investigation of the effects of WKYMVm, a selective FPR2 agonist isolated by screening synthetic peptide libraries, on homing ability of ECFCs and vascular regeneration of ischemic tissues suggests that WKYVm promotes repair of isChemic tissues by stimulating homing of EC FCs and neovascularization via a F PR2‐dependent mechanism.
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Hypoxia Inhibits Cellular Senescence to Restore the Therapeutic Potential of Old Human Endothelial Progenitor Cells via the Hypoxia-Inducible Factor-1α–TWIST-p21 Axis

TL;DR: Ex vivo expansion protocols involving hypoxic preconditioning that are suitable for efficiently expanding old EPCs without senescence through modulation of the hypoxia-induced hypoxIA-inducible factor-1&agr;–TWIST-p21 axis are introduced.
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The effects of flap ischemia on normal and diabetic progenitor cell function.

TL;DR: The vasculogenic potential of endothelial progenitor cells at various stages of differentiation is impaired in diabetes and thus may account for impaired ischemia-induced vasculogenesis observed clinically.