M
Michael A. Ihnat
Researcher at University of Oklahoma Health Sciences Center
Publications - 90
Citations - 4498
Michael A. Ihnat is an academic researcher from University of Oklahoma Health Sciences Center. The author has contributed to research in topics: Receptor tyrosine kinase & Growth factor receptor. The author has an hindex of 32, co-authored 87 publications receiving 4019 citations. Previous affiliations of Michael A. Ihnat include Duquesne University & University of Oklahoma.
Papers
More filters
Journal ArticleDOI
Oscillating glucose is more deleterious to endothelial function and oxidative stress than mean glucose in normal and type 2 diabetic patients
Antonio Ceriello,Katherine Esposito,Ludovica Piconi,Michael A. Ihnat,Jessica E. Thorpe,Roberto Testa,Massimo Boemi,Dario Giugliano +7 more
TL;DR: It is suggested that oscillating glucose can have more deleterious effects than constant high glucose on endothelial function and oxidative stress, two key players in favoring cardiovascular complications in diabetes.
Journal ArticleDOI
The "metabolic memory": is more than just tight glucose control necessary to prevent diabetic complications?
TL;DR: The emergence of this metabolic memory suggests the need for early aggressive treatment aiming to "normalize" metabolic control together perhaps with the addition of agents which reduce cellular reactive species and glycation in order to minimize long-term diabetic complications.
Journal ArticleDOI
Novel STAT3 Phosphorylation Inhibitors Exhibit Potent Growth-Suppressive Activity in Pancreatic and Breast Cancer Cells
Li Lin,Brian Hutzen,Mingxin Zuo,Sarah Ball,Stephanie Deangelis,Elizabeth Foust,Bulbul Pandit,Michael A. Ihnat,Satyendra S. Shenoy,Samuel K. Kulp,Pui-Kai Li,Chenglong Li,James R. Fuchs,Jiayuh Lin +13 more
TL;DR: FLLL31 and FLLL32 are effective inhibitors of STAT3 phosphorylation, DNA-binding activity, and transactivation in vitro, leading to the impediment of multiple oncogenic processes and the induction of apoptosis in pancreatic and breast cancer cell lines.
Journal ArticleDOI
‘Glycaemic variability’: a new therapeutic challenge in diabetes and the critical care setting
TL;DR: In this paper, it was shown that oscillating glucose is more dangerous than stable constant high glucose, particularly in activating the pathways involved in the pathogenesis of diabetes complications, and the production of free radicals, accompanied by an insufficient increase in intracellular antioxidant defences, seems to account for this phenomenon.
Journal ArticleDOI
Reactive oxygen species mediate a cellular ‘memory’ of high glucose stress signalling
Michael A. Ihnat,Jessica E. Thorpe,Chandrashekhar D. Kamat,Csaba Szabó,Dixy E. Green,Linda A. Warnke,Z. Lacza,A. Cselenyák,K. Ross,S. Shakir,Ludovica Piconi,R. C. Kaltreider,Antonio Ceriello +12 more
TL;DR: These results provide proof-of-principle of a ROS-mediated cellular persistence of vascular stress after glucose normalisation, and were obtained in the retina of diabetic rats with α-lipoic acid added to the last week of normalised glucose.