H
Heberty T. Facundo
Researcher at University of Louisville
Publications - 38
Citations - 1417
Heberty T. Facundo is an academic researcher from University of Louisville. The author has contributed to research in topics: Mitochondrion & Mitochondrial permeability transition pore. The author has an hindex of 16, co-authored 30 publications receiving 1248 citations. Previous affiliations of Heberty T. Facundo include Duke University & Federal University of Ceará.
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Journal ArticleDOI
O-linked β-N-acetylglucosamine transferase is indispensable in the failing heart
Lewis J. Watson,Heberty T. Facundo,Gladys A. Ngoh,Mohamed Ameen,Robert E. Brainard,Kewakebt M. Lemma,Bethany W. Long,Sumanth D. Prabhu,Yu-Ting Xuan,Steven P. Jones +9 more
TL;DR: Data provided provide keen insights into the pathophysiology of the failing heart and illuminate a previously unrecognized point of integration between metabolism and cardiac function in the failingheart.
Journal ArticleDOI
O-GlcNAc Signaling in the Cardiovascular System
TL;DR: Evidence of protein O-GlcNAcylation as an autoprotective alarm or stress response in the cardiovascular system is highlighted and recent literature supporting the idea that promoting O- GlcNA Cylation improves cell survival during acute stress, whereas limiting it exacerbates cell damage in similar models is discussed.
Journal ArticleDOI
Augmented O-GlcNAc signaling attenuates oxidative stress and calcium overload in cardiomyocytes
TL;DR: Inhibition of Ca2+ overload and ROS generation (inducers of mPTP) might be one mechanism through which O-GlcNAcylation reduces ischemia/hypoxia-mediated m PTP formation.
Journal ArticleDOI
Mitochondrial ATP-sensitive K+ channels are redox-sensitive pathways that control reactive oxygen species production.
TL;DR: It is demonstrated that mitoK(ATP) channel activity effectively prevents mitochondrial reactive oxygen release and acts as a reactive oxygen sensor that decreases mitochondrial free radical generation in response to enhanced local levels of oxidants.
Journal ArticleDOI
Unique Hexosaminidase Reduces Metabolic Survival Signal and Sensitizes Cardiac Myocytes to Hypoxia/ Reoxygenation Injury
Gladys A. Ngoh,Heberty T. Facundo,Tariq Hamid,Wolfgang H. Dillmann,Natasha E. Zachara,Steven P. Jones,Steven P. Jones +6 more
TL;DR: The present results provide definitive evidence that O-GlcNAcase antagonizes posthypoxic cardiac myocyte survival and support a renewed approach to the contribution of metabolism and metabolic signaling to the determination of cell fate.