Guillermo Vazquez
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Professor (with tenure)
Program Director MSBS-Medical Sciences
Associate Director, Center for Hypertension and Precision Medicine, Physiology and Pharmacology , College of Medicine and Life Sciences
Overview
overview
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Dr. Vazquez completed his undergraduate and doctoral studies in Biochemistry at the National University of the South in Argentina, earning his Ph.D. in 1997. He pursued advanced training as a von Humboldt Visiting Fellow in Pharmacology at the Freie Universität in Berlin, Germany (1997), followed by a Visiting Postdoctoral Fellowship in the Signal Transduction Division at the National Institute of Environmental Health Sciences in North Carolina (2001–2006).
He joined the University of Toledo College of Medicine and Life Sciences (UTCOMLS) in 2007, where he is now a tenured Professor in the Department of Physiology and Pharmacology. He also serves as Associate Director of the Center for Hypertension and Precision Medicine and Director of the MSBS in Medical Sciences program.
For the past 18 years, Dr. Vazquez has combined a strong record of teaching and mentoring with an independent, AHA- and NIH-funded research program investigating the molecular and cellular basis of coronary heart disease. His pioneering studies on the role of TRPC channels in endothelial and macrophage biology have led to important insights into mechanisms of vascular dysfunction and atherosclerosis, with publications in high-impact scientific journals. His scientific contributions have been recognized through election as a Fellow of the American Heart Association, as well as institutional honors such as the Dean’s New Investigator Award and the Dean’s Mentor Award.
In addition to his research accomplishments, Dr. Vazquez has established himself as an educational leader and innovator. As Director of the MSBS in Medical Sciences program, he has spearheaded initiatives that enhance advising, curricular alignment, and student success. He developed and implemented a centralized advising model endorsed by college leadership, designed the innovative MSBS Flex pathway to meet the needs of diverse student populations, and expanded opportunities for professional development through seminars and alumni engagement. Under his leadership, the MSBS program has grown in quality, visibility, and impact as a pipeline to medical and health professional schools.
Dr. Vazquez continues to integrate scholarship, teaching, and program innovation to advance both biomedical education and cardiovascular science, making lasting contributions to the mission of the University of Toledo and to the broader academic community.
Publications
selected publications
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Article (Faculty180)
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Pleiotropic Effect of a High Resolution Mapped Blood Pressure QTL on Tumorigenesis. PloS one. 11:e0153519.
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Role of Canonical Transient Receptor Potential (trpc) Channels in Receptor-dependent Regulation of Vascular Cell Adhesion Molecule-1 in Human Coronary Artery Endothelium: P229. Arteriosclerosis, Thrombosis, and Vascular Biology. e.
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Stimulation of Ca2+ release-activated Ca2+ channels as a potential mechanism involved in non-genomic 1, 25 (OH) 2-vitamin D3-induced Ca2+ entry in skeletal muscle cells. Biochemical and biophysical research communications. 562.
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Article (Web of Science)
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2020Loss of Hepatic Carcinoembryonic Antigen-Related Cell Adhesion Molecule 1 Links Nonalcoholic Steatohepatitis to Atherosclerosis. HEPATOLOGY COMMUNICATIONS.Full Text via DOI: 10.1002/hep4.1590
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2019CACNB2 is associated with aberrant RAS-MAPK signaling in hypertensive Dahl Salt-Sensitive rats. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS. 513:760-765.Full Text via DOI: 10.1016/j.bbrc.2019.03.215 PMID: 30992131
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2018Attenuation of Microbiotal Dysbiosis and Hypertension in a CRISPR/Cas9 Gene Ablation Rat Model of GPER1. HYPERTENSION. 72:1125-1132.Full Text via DOI: 10.1161/HYPERTENSIONAHA.118.11175
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2018Liver-specific rescuing of CEACAM1 reverses endothelial and cardiovascular abnormalities in male mice with null deletion of Ceacam1 gene. MOLECULAR METABOLISM. 9:98-113.Full Text via DOI: 10.1016/j.molmet.2018.01.009
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2018Reduced calcification and osteogenic features in advanced atherosclerotic plaques of mice with macrophage-specific loss of TRPC3. ATHEROSCLEROSIS. 270:199-204.Full Text via DOI: 10.1016/j.atherosclerosis.2017.12.025
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2018Attenuation of Microbiotal Dysbiosis and Hypertension in a CRISPR/Cas9 Gene Ablation Rat Model of GPER1. HYPERTENSION. 72:1125-1132.Full Text via DOI: 10.1161/hypertensionaha.118.11175
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2017Evidence for constitutive bone morphogenetic protein-2 secretion by M1 macrophages: Constitutive auto/paracrine osteogenic signaling by BMP-2 in M1 macrophages. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS. 491:154-158.Full Text via DOI: 10.1016/j.bbrc.2017.07.065
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2017Reduced Necrosis and Content of Apoptotic M1 Macrophages in Advanced Atherosclerotic Plaques of Mice With Macrophage-Specific Loss of Trpc3. SCIENTIFIC REPORTS. 7.Full Text via DOI: 10.1038/srep42526
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2017Deep Transcriptomic Profiling of M1 Macrophages Lacking Trpc3. SCIENTIFIC REPORTS. 7.Full Text via DOI: 10.1038/srep39867
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2016Early steatohepatitis in hyperlipidemic mice with endothelial-specific gain of TRPC3 function precedes changes in aortic atherosclerosis. PHYSIOLOGICAL GENOMICS. 48:644-649.Full Text via DOI: 10.1152/physiolgenomics.00067.2016
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2016Pleiotropic Effect of a High Resolution Mapped Blood Pressure QTL on Tumorigenesis. PLOS ONE. 11.Full Text via DOI: 10.1371/journal.pone.0153519
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2016On the Roles of the Transient Receptor Potential Canonical 3 (TRPC3) Channel in Endothelium and Macrophages: Implications in Atherosclerosis. CALCIUM ENTRY PATHWAYS IN NON-EXCITABLE CELLS. 898:185-199.Full Text via DOI: 10.1007/978-3-319-26974-0_9
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2016Pharmacological evidence for a role of the transient receptor potential canonical 3 (TRPC3) channel in endoplasmic reticulum stress-induced apoptosis of human coronary artery endothelial cells. VASCULAR PHARMACOLOGY. 76:42-52.Full Text via DOI: 10.1016/j.vph.2015.07.011
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2015Increased size and cellularity of advanced atherosclerotic lesions in mice with endothelial overexpression of the human TRPC3 channel. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA. 112:E2201-E2206.Full Text via DOI: 10.1073/pnas.1505410112
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2014Reduced endoplasmic reticulum stress-induced apoptosis and impaired unfolded protein response in TRPC3-deficient M1 macrophages. AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY. 307:C521-C531.Full Text via DOI: 10.1152/ajpcell.00369.2013
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2014Bone marrow deficiency of TRPC3 channel reduces early lesion burden and necrotic core of advanced plaques in a mouse model of atherosclerosis. CARDIOVASCULAR RESEARCH. 101:138-144.Full Text via DOI: 10.1093/cvr/cvt231
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2013Ceacam1 deletion causes vascular alterations in large vessels. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM. 305:E519-E529.Full Text via DOI: 10.1152/ajpendo.00266.2013
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2013Evidence for a prosurvival role of alpha-7 nicotinic acetylcholine receptor in alternatively (M2)-activated macrophages. PHYSIOLOGICAL REPORTS. 1:e00189.Full Text via DOI: 10.1002/phy2.189
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2012Involvement of calmodulin and calmodulin kinase II in tumor necrosis factor alpha-induced survival of bone marrow derived macrophages. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS. 427:178-184.Full Text via DOI: 10.1016/j.bbrc.2012.09.038
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2011Evidence for Operation of Nicotinic and Muscarinic Acetylcholine Receptor-Dependent Survival Pathways in Human Coronary Artery Endothelial Cells. JOURNAL OF CELLULAR BIOCHEMISTRY. 112:1978-1984.Full Text via DOI: 10.1002/jcb.23169
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2011Impairment of survival signaling and efferocytosis in TRPC3-deficient macrophages. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS. 410:643-647.Full Text via DOI: 10.1016/j.bbrc.2011.06.045
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2011Requirement for non-regulated, constitutive calcium influx in macrophage survival signaling. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS. 407:432-437.Full Text via DOI: 10.1016/j.bbrc.2011.03.048
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2010The Constitutive Function of Native TRPC3 Channels Modulates Vascular Cell Adhesion Molecule-1 Expression in Coronary Endothelial Cells Through Nuclear Factor kappa B Signaling. CIRCULATION RESEARCH. 106:1479-1488.Full Text via DOI: 10.1161/CIRCRESAHA.109.213314
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2010The Constitutive Function of Native TRPC3 Channels Modulates Vascular Cell Adhesion Molecule-1 Expression in Coronary Endothelial Cells Through Nuclear Factor κB Signaling. CIRCULATION RESEARCH. 106:1479-1488.Full Text via DOI: 10.1161/circresaha.109.213314
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2008Involvement of Native TRPC3 Proteins in ATP-Dependent Expression of VCAM-1 and Monocyte Adherence in Coronary Artery Endothelial Cells. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY. 28:2049-2055.Full Text via DOI: 10.1161/ATVBAHA.108.175356
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2008Involvement of Native TRPC3 Proteins in ATP-Dependent Expression of VCAM-1 and Monocyte Adherence in Coronary Artery Endothelial Cells. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY. 28:2049-2055.Full Text via DOI: 10.1161/atvbaha.108.175356
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Meeting Abstract (Web of Science)
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2009Upregulated Expression of Constitutively Active Transient Receptor Potential Canonical 3 Channels in Coronary Endothelial Cells Modulates Vascular Cell Adhesion Molecule-1 Expression and Monocyte Adhesion. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY. E111-E111.
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Proceedings (Faculty180)
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Review Article (Web of Science)
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2012Macrophage function in atherosclerosis Potential roles of TRP channels. CHANNELS. 141-148.Full Text via DOI: 10.4161/chan.20292
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2010On the potential role of source and species of diacylglycerol in phospholipase-dependent regulation of TRPC3 channels. CHANNELS. 232-240.Full Text via DOI: 10.4161/chan.4.3.12058
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Contact
full name
- Guillermo Vazquez