Zobrazeno 1 - 10
of 12
pro vyhledávání: '"William R Urciuoli"'
Autor:
Andrew P Wojtovich, Teresa A Sherman, Sergiy M Nadtochiy, William R Urciuoli, Paul S Brookes, Keith Nehrke
Publikováno v:
PLoS ONE, Vol 6, Iss 12, p e28287 (2011)
Mitochondrial potassium channels are important mediators of cell protection against stress. The mitochondrial large-conductance "big" K(+) channel (mBK) mediates the evolutionarily-conserved process of anesthetic preconditioning (APC), wherein exposu
Externí odkaz:
https://doaj.org/article/df446d12a17047628ab10422eff63521
Autor:
Andrew P. Wojtovich, Sergiy M. Nadtochiy, William R. Urciuoli, Charles O. Smith, Morten Grunnet, Keith Nehrke, Paul S. Brookes
Publikováno v:
PeerJ, Vol 1, p e48 (2013)
Opening of BK-type Ca2+ activated K+ channels protects the heart against ischemia-reperfusion (IR) injury. However, the location of BK channels responsible for cardioprotection is debated. Herein we confirmed that openers of the SLO1 BK channel, NS16
Externí odkaz:
https://doaj.org/article/068a80317fd54b418b5dd6c90912c59c
Publikováno v:
American Journal of Physiology-Heart and Circulatory Physiology. 306:H1602-H1609
Ischemia-reperfusion (IR) injury is significantly worse in aged hearts, but the underlying mechanisms are poorly understood. Age-related damage to mitochondria may be a critical feature, which manifests in an exacerbation of IR injury. Silent informa
Autor:
C. Owen Smith, Paul S. Brookes, Yves T. Wang, Andrew P. Wojtovich, Keith Nehrke, Xiao Ming Xia, William R. Urciuoli
Publikováno v:
Anesthesiology. 124(5)
BackgroundAnesthetic preconditioning (APC) is a clinically important phenomenon in which volatile anesthetics (VAs) protect tissues such as heart against ischemic injury. The mechanism of APC is thought to involve K+ channels encoded by the Slo gene
Autor:
Andrew M. Walters, Stefanie Devito, Andrew P. Wojtovich, Paul S. Brookes, Adam J. Olm-Shipman, Stephanie Guo, William R. Urciuoli, Sergiy M. Nadtochiy
Publikováno v:
Circulation Research. 110:948-957
Rationale: Tissue ischemia/reperfusion (IR) injury underlies several leading causes of death such as heart-attack and stroke. The lack of clinical therapies for IR injury may be partly due to the difficulty of adapting IR injury models to high-throug
Mitochondrial quality control mechanisms have been implicated in protection against cardiac ischemia-reperfusion (IR) injury. Previously, cloxyquin (5-chloroquinolin-8-ol) was identified via phenotypic screening as a cardioprotective compound. Herein
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::6980d0807419108db66115a327572493
https://europepmc.org/articles/PMC4796459/
https://europepmc.org/articles/PMC4796459/
Publikováno v:
Circulation Research. 117
Introduction: SIRT3 is a mitochondrial metabolic regulator, and a decline in function of SIRT3 may play a role in age-related mitochondrial alterations. The aim of this study was to investigate the possible down-regulation of SIRT3 activity in aged h
Autor:
Andrew P Wojtovich, C O Smith, Sergiy M Nadtochiy, William R Urciuoli, Xiao-Ming Xia, Elizabeth Jonas, Christopher J Lingle, Keith Nehrke, Paul S Brookes
Publikováno v:
Circulation Research. 115
Introduction: Volatile anesthetic preconditioning (APC) protects the heart from ischemia-reperfusion (IR) injury. APC elicits evolutionarily-conserved protective signaling pathways that converge at the mitochondrial level, where the Slo family of K +
Publikováno v:
Circulation Research. 115
Introduction: SIRT3 deficiency leads to increased mitochondrial acetylation, and enhances sensitivity of the heart to stress. Recently we demonstrated that a worse outcome of ischemia-reperfusion (IR) injury in aged hearts was associated with increas
Autor:
Aron B. Fisher, Shampa Chatterjee, Andrew P. Wojtovich, Paul S. Brookes, Keith Nehrke, William R. Urciuoli
Publikováno v:
American journal of physiology. Heart and circulatory physiology. 304(11)
ATP-sensitive K+ (KATP) channels that contain K+ inward rectifier subunits of the 6.2 isotype (Kir6.2) are important regulators of the cardiac response to ischemia-reperfusion (I/R) injury. Opening of these channels is implicated in the cardioprotect