Scott M. Moore
University of North Carolina at Chapel Hill
7 Papers
5 Citations
Scott M. Moore is an academic researcher from University of North Carolina at Chapel Hill. The author has contributed to research in topics: Collateral circulation & Ischemia. The author has an hindex of 5, co-authored 7 publications.
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Papers
Lysine Acetyltransferase PCAF Is a Key Regulator of Arteriogenesis
A.J.N.M. Bastiaansen,M.M. Ewing,Hetty C. de Boer,Tineke C. T. M. van der Pouw Kraan,Margreet R. de Vries,Erna Peters,Sabine M.J. Welten,Ramon Arens,Scott M. Moore,James E. Faber,J. Wouter Jukema,Jaap F. Hamming,A. Yaël Nossent,Paul H.A. Quax +13 more
TL;DR: Findings indicate that PCAF acts as master switch in the inflammatory processes required for effective arteriogenesis, indicating that modulation of factors that act as a master switch for relevant gene programs may prove more effective.
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A method for evaluating the murine pulmonary vasculature using micro-computed tomography.
Michael R. Phillips,Scott M. Moore,Mansi Shah,Clara N. Lee,Yueh Z. Lee,James E. Faber,Sean E. McLean +6 more
TL;DR: Robust high-resolution segmentation was achieved, permitting detailed quantitation of pulmonary vascular morphometrics in postnatal and adult mice, and as expected, postnatal lung development was associated with progressive increase in small-vessel number and arterial branching complexity.
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•Journal Article
Abstract 390: Cardiovascular Risk Factors and Endothelial Dysfunction Cause Rarefaction of the Collateral Circulation and Impaired Recovery from Ischemia
TL;DR: Examination of recovery of perfusion following femoral artery ligation and native cerebral pial collateral extent in mouse models shows that CVRF not only impair collateral remodeling but also cause significant loss of native collaterals, resulting in worse ischemic tissue injury after acute obstruction and fewer collateral available for remodeling.
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Cardiovascular risk factors cause premature rarefaction of the collateral circulation and greater ischemic tissue injury
TL;DR: Chronic CVRF presence caused collateral rarefaction and worse ischemic injury, even at relatively young ages and was associated with increased proliferation rate of collateral endothelial cells, effects that may promote accelerated endothelial cell senescence.