Gabor Csanyi, Ph.D.
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Pagano Lab |
Bio
Dr. Csanyi earned his MPharm from the University of Szeged, Hungary in 2003 and followed this with a PhD from the same institution in 2008. He has also studied at Jagiellonian University Medical College, Krakow, Poland. After a brief period in the Pagano laboratory at Henry Ford Hospital in Detroit, Dr. Csanyi moved to the University of Pittsburgh to continue his postdoctoral fellowship in the summer of 2008.
Research Interests
A large body of literature supports the importance of NADPH oxidase-derived reactive oxygen species (ROS) in the pathophysiology of cardiovascular disorders. Dr. Csanyi's research is directed toward a better understanding of the role of distinct vascular isoforms of NADPH oxidase (Nox1, Nox2, Nox4, and Nox5) and increased ROS production in the initiation and progression of vascular disease. During the course of his postdoctoral training, Dr. Csanyi has been intrigued by how the matricellular protein thrombospondin-1 (TSP1) regulates nitric oxide (NO) signaling in vascular disease. Dr. Csanyi has recently demonstrated that TSP1 is a rapid and robust activator of Nox1 in vascular cells and an important regulator of NO bioavailability. Since these original findings, Dr. Csanyi has developed an independent pathway that merges the two distinct fields of NADPH oxidase- and TSP1-signaling in vascular inflammatory diseases. His short-term goal is to develop this project into a unique research program expanding on this seminal discovery with high impact contributions to our mechanistic understanding of the factors controlling this novel pathway. Longer term, a broader vision for his work is the interrogation of the myriad ways matricellular proteins could affect phenotypic changes in macrophages, T cells, and vascular parenchymal cells, leading to vascular disease.
Key Publications
Csányi G and Pagano PJ. Strategies Aimed at Nox4 Oxidase Inhibition Employing Peptides from Nox4 B-Loop and C-Terminus and p22 (phox) N-Terminus: An Elusive Target. Int J Hypertens. 2013:842827. (2013).
Csányi G, Yao M, Rodriguez AI, Al Ghouleh I, Sharifi-Sanjani M, Frazziano G, Huang X, Kelley EE, Isenberg JS, Pagano PJ. Thrombospondin-1 regulates blood flow via CD47 receptor-mediated activation of NADPH oxidase 1. Arterioscler Thromb Vasc Biol. 32(12):2966-73. (2012).
Csányi G, Gajda M, Franczyk-Zarow M, Kostogrys R, Gwozdź P, Mateuszuk L, Sternak M, Wojcik L, Zalewska T, Walski M, Chlopicki S. Functional alterations in endothelial NO, PGI2 and EDHF pathways in aorta in apoE/LDLR-/- mice. Prostaglandins Other Lipid Mediat. 98(3-4):107-15 (2012).
Csányi G, Cifuentes-Pagano E, Al Ghouleh I, Ranayhossaini DJ, Egaña L, Lopes LR, Jackson HM, Kelley EE, Pagano PJ. Nox2 B-loop peptide, Nox2ds, specifically inhibits the NADPH oxidase Nox2. Free Radic Biol Med. 51:1116-25 (2011).
Cascino T, Csányi G, Al Ghouleh I, Montezano AC, Touyz RM, Haurani MJ, Pagano PJ. Adventitia-derived hydrogen peroxide impairs relaxation of the rat carotid artery via smooth muscle cell p38 mitogen-activated protein kinase. Antioxid Redox Signal. 15:1507-15 (2011).
Csányi G, Taylor RW, Pagano PJ. NOX and inflammation in the vascular adventitia. Free Rad Biol Med. 47:1254-66 (2009).
Csányi G, Kis B, Gecse A, Telegdy G, Szupera Z, Vécsei L, Szente M, Leprán I, Mezei Z. Effects of 3-aminopyridine-induced seizures on platelet eicosanoid synthesis. Pharmacol Rep. 60:345-352 (2008).
Csányi G, Lepran I, Flesch T, Telegdy G, Szabo G, Mezei Z. Lack of endothelium-derived hyperpolarizing factor (EDHF) up-regulation in endothelial dysfunction in aorta in diabetic rats. Pharmacol Rep. 59:447-455 (2007).
Jawien J, Csányi G, Gajda M, Mateuszuk L, Lomnicka M, Korbut R, Chlopicki S. Ticlopidine attenuates progression of atherosclerosis in apolipoprotein E and low density lipoprotein receptor double knockout mice. Eur J Pharmacol. 556:129-135 (2007).
Csányi G, Bauer M, Dietl W, Lomnicka M, Stepuro T, Podesser BK, Chlopicki S. Functional alterations in NO, PGI2 and EDHF pathways in the aortic endothelium after myocardial infarction in rats. Eur J Heart Fail. 8:769-776 (2006).
Honors, Awards, and Organizations
| 2003 | Eutimia-award, First prize for Best Oral Presentation, Szeged, Hungary |
| 2003 | First Prize, Scientific Research Student Congress, Szeged, Hungary |
| 2004-2005 | Jozef Dietl Academic Scholarship, Krakow, Poland |
| 2007 | Queen Jadwiga Fund, Krakow, Poland |
| 2008 | Ph.D. University of Szeged, Hungary - Summa Cum Laude |
| 2009-2012 | Member, Society for Free Radical Biology and Medicine (SFRBM) |
| 2009 | Young Investigator Award, SFRBM, San Francisco, CA, USA |
| 2010 | Young Investigator Award, SFRBM, Orlando, FL, USA |
| 2010-2012 | Great Rivers Affiliate Postdoctoral Fellowship, AHA (10POST3030009) |
| 2010-Present | Coordinator of Vascular Medicine Institute’s Postdoctoral Journal Club |
| 2011 | Member of SFRBM Junior Awards Committee |
| 2011-Present | Reviewer of Antioxidants & Redox Signaling |
| 2012 | New Investigator Travel Award, AHA’s Council for High Blood Pressure Research |
| 2012-Present | Member of the American Heart Association |
| 2012-Present | Member of International Atherosclerotic Society |
| 2012 | Guest-Editor; Oxidative Stress in Vascular Disease Special Issue; International Journal of Molecular Sciences |
Research Support
Pending Research Support
NIH Pathway to Independence Award (K99/R00) (1K99HL114648-01A1); Csanyi (PI)
Completed Research Support
American Heart Association, Great Rivers Affiliate Postdoctoral Fellowship (10POST3030009); 1 Jul 2010-30 Jun 2012; Csanyi (PI); This proposal investigated whether TSP1 increases reactive oxygen species production in vascular smooth muscle cells.
Queen Jadwiga Fund, Jagiellonian University Medical College, Predoctoral fellowship; 1 Nov 2007-31 Jan 2008; Csanyi (PI); This proposal studied alterations in endothelium-derived hyperpolarizing factor-mediated relaxation in atherosclerosis.
Jozef Dietl Academic Scholarship, Jagiellonian University Medical College, Predoctoral fellowship; 1 Oct 2004-30 Sep 2005; Csanyi (PI); This proposal studied the role nitric oxide- and prostacyclin-dependent endothelial function in ischemic heart failure.
Pubmed link
