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Steven Lentz

Professor,  Internal Medicine

Contact Information

Phone: +1 319 356 4048
Email: steven-lentz@uiowa.edu


MD, Washington University
PhD, Molecular Biology, Washington University
Residency, Barnes Hospital
Fellowship, Washington University


Primary: Internal Medicine
Secondary: Biomedical Engineering

Centers and Program Affiliations

Interdisciplinary Graduate Program in Molecular and Cellular Biology

Research Interests

MeSH Terms from Publications

Research Summary

The major focus of research in Dr. Lentz's laboratory is endothelial function in vascular diseases and tissue injury, with particular emphasis on structure, function, and regulation of hemostatic proteins. Dr. Lentz’s laboratory utilizes molecular and cellular techniques, along with transgenic and gene targeted animals, to investigate the mechanisms of regulation of hemostasis by vascular cells such as endothelium, vascular muscle, and platelets. The long-term goals of the laboratory are to define the molecular and cellular interactions that regulate vascular function and to identify the key mechanisms of impairment of vascular function in disease states such as hyperhomocysteinemia and atherosclerosis. Dr. Lentz also directs a clinical research program in hemophilia and thrombophilia and is a member of the Executive Committee of the the NCI-funded University of Iowa Lymphoma SPORE. Current areas of investigation include the following:

Vascular function in hyperhomocysteinemia and atherosclerosis.  A high blood level of the sulfur-containing amino acid, homocysteine, is a risk factor for cardiovascular disease, stroke, venous thromboembolism, and vascular dementia. This condition is called hyperhomocysteinemia. We are using molecular genetic approaches to define the mechanisms of vascular dysfunction and accelerated thrombosis in hyperhomocysteinemia. Current projects are investigating the role of reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress, and the signaling pathways that provide protection from cellular stress. We also use genetic approaches to investigate mechanisms of altered endothelial regulation of hemostatic function, including impairment of the thrombomodulin/protein C anticoagulant pathway during atherosclerosis and regression of atherosclerosis.

Platelet procoagulant activity.  We have developed methods to study platelet activation and the generation of platelet procoagulant activity in mice. We are currently are using genetic approaches in mice to further define the signal transduction pathways responsible for platelet procoagulant activity.
Hemophilia and thrombosis.  Under the direction of Dr. Lentz, the Iowa Hemophilia and Thrombosis Center conducts a broad program of clinical trials in hemophilia and venous thromboembolism.

Recent Publications

Show publications
  1. ADAMTS13 reduces VWF-mediated acute inflammation following focal cerebral ischemia in mice. J Thromb Haemost 10(8):1665-71, 2012. [PubMed]
  2. Critical von Willebrand factor A1 domain residues influence type VI collagen binding. J Thromb Haemost 10(7):1417-24, 2012. [PubMed]
  3. Alternatively-spliced extra domain A of fibronectin promotes acute inflammation and brain injury after cerebral ischemia in mice. Stroke 43(5):1376-82, 2012. [PubMed]
  4. Paradoxical absence of a prothrombotic phenotype in a mouse model of severe hyperhomocysteinemia. Blood 119(13):3176-83, 2012. [PubMed]
  5. ADAMTS13 reduces vascular inflammation and the development of early atherosclerosis in mice. Blood 119(10):2385-91, 2012. [PubMed]
  6. Recombinant factor VIIa analog (vatreptacog alfa [activated]) for treatment of joint bleeds in hemophilia patients with inhibitors: a randomized controlled trial. J Thromb Haemost 10(1):81-9, 2012. [PubMed]
  7. Human thrombomodulin knock-in mice reveal differential effects of human thrombomodulin on thrombosis and atherosclerosis. Arterioscler Thromb Vasc Biol 31(11):2509-17, 2011. [PubMed]
  8. Durable responses to rituximab in acquired factor VIII deficiency. Thromb Haemost 106(1):172-4, 2011. [PubMed]
  9. Epigenetic regulation of hepatic endoplasmic reticulum stress pathways in the ethanol-fed cystathionine beta synthase-deficient mouse. Hepatology 51(3):932-41, 2010. [PubMed]
  10. The nutrigenetics of hyperhomocysteinemia: quantitative proteomics reveals differences in the methionine cycle enzymes of gene-induced versus diet-induced hyperhomocysteinemia. Mol Cell Proteomics 9(3):471-85, 2010. [PubMed]