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Steven Poelzing, Ph.D.

Steven Poelzing, Ph.D.

Associate Professor

Steven Poelzing, Ph.D.-lab shot

“Understanding what channels cells use to communicate provides the basis for developing new treatments and medications to address common ailments, such as ischemic heart disease, arrhythmias, and sudden cardiac death due to congenital disease.”

Solving the mystery of sudden cardiac death

What causes the heart's electrical system to malfunction?

Scientists are increasingly aware that sudden cardiac death — a significant cause of mortality in the United States and around the world — is linked to genetic mutations in cardiac proteins, or changes in those same proteins during diseases such as heart failure, ischemia, or diabetes.

One cardiac gap junction protein of interest, Connexin43, or Cx43, allows the spread of electrical activity between cardiac myocytes to coordinate uniform, synchronized contraction. Conventional theory suggests that reducing Cx43 expression slows the spread of electrical activity — conduction — in the heart and increases risk of arrhythmias leading to sudden death. The experimental relationships between conduction slowing, sudden cardiac death, and loss of Cx43 are not straightforward. Conflicting findings have led to a lack of experimental agreement on the degree of conduction slowing expected from a quantifiable reduction of Cx43.

Poelzing hypothesizes that the spread of electrical activity between cardiac myocytes is not only mediated through connexins, but also through electric fields between myocytes. His laboratory has demonstrated that the hydration state of the heart can mask or unmask conduction slowing in the presence of reduced Cx43 expression. Poelzing seeks to determine how pathological insults such as cardiac inflammation and edema modulate the risk of sudden death in the young and how age changes this relationship.

  • Associate Professor, Fralin Biomedical Research Institute at VTC
  • Associate Professor, Department of Biomedical Engineering and Mechanics, College of Engineering
  • Associate Professor, Department of Internal Medicine, School of Medicine
  •  Co-Director, Translational Biology, Medicine, and Health Graduate Program

Nowak MB, Poelzing S, Weinberg SH. Mechanisms underlying age-associated manifestation of cardiac sodium channel gain-of-function. J Mol Cell Cardiol. 2020 Dec 26;153:60-71. doi: 10.1016/j.yjmcc.2020.12.008. [Epub ahead of print] PubMed PMID: 33373643; NIHMSID:NIHMS1659961.

Nowak MB, Greer-Short A, Wan X, Wu X, Deschênes I, Weinberg SH, Poelzing S. Intercellular Sodium Regulates Repolarization in Cardiac Tissue with Sodium Channel Gain of Function. Biophys J. 2020 Jun 2;118(11):2829-2843. doi: 10.1016/j.bpj.2020.04.014. Epub 2020 Apr 21. PubMed PMID: 32402243; PubMed Central PMCID: PMC7264809.

Schultz F, Swiatlowska P, Alvarez-Laviada A, Sanchez-Alonso JL, Song Q, de Vries AAF, Pijnappels DA, Ongstad E, Braga VMM, Entcheva E, Gourdie RG, Miragoli M, Gorelik J. Cardiomyocyte-myofibroblast contact dynamism is modulated by connexin-43. FASEB J. 2019 Sep;33(9):10453-10468. doi: 10.1096/fj.201802740RR. Epub 2019 Jul 5. PubMed PMID: 31253057; PubMed Central PMCID: PMC6704460.

Jiang J, Hoagland D, Palatinus JA, He H, Iyyathurai J, Jourdan LJ, Bultynck G, Wang Z, Zhang Z, Schey K, Poelzing S, McGowan FX, Gourdie RG. Interaction of α Carboxyl Terminus 1 Peptide With the Connexin 43 Carboxyl Terminus Preserves Left Ventricular Function After Ischemia-Reperfusion Injury. J Am Heart Assoc. 2019 Aug 20;8(16):e012385. doi: 10.1161/JAHA.119.012385. Epub 2019 Aug 19. PubMed PMID: 31422747; PubMed Central PMCID: PMC6759879.

George SA, Hoeker G, Calhoun PJ, Entz M 2nd, Raisch TB, King DR, Khan M, Baker C, Gourdie RG, Smyth JW, Nielsen MS, Poelzing S. Modulating cardiac conduction during metabolic ischemia with perfusate sodium and calcium in guinea pig hearts. Am J Physiol Heart Circ Physiol. 2019 Apr 1;316(4):H849-H861. doi: 10.1152/ajpheart.00083.2018. Epub 2019 Feb 1. PubMed PMID: 30707595; PubMed Central PMCID: PMC6483020.



  • University of Utah, Research Associate Professor, Bioengineering
  • NASA Glenn Research Center, Consultant
  • Case Western Reserve University, Research Assistant
  • Wright State University, National Science Foundation Research Fellow

 

  • MetroHealth Medical Center, Postdoctoral fellowship
  • Case Western Reserve University, Ph.D., Biomedical Engineering
  • Case Western Reserve University, MSE, Biomedical Engineering
  • Wright State University, B.S., Biomedical Engineering
  • Fellow, Heart Rhythm Society, 2015
  • Fellow, American Heart Association, 2014
  • Editorial Board, Frontiers in Cardiac Electrophysiology editorial board, 2010-Present
  • Top Instructors in Engineering, University of Utah, 2008, 2009, 2010, 2011
  • Michael Bilitch Fellowship in Cardiac Pacing and Electrophysiology, Heart Rhythm Society, 2004



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