Drew Nassal

About

Drew Nassal, PhD, is an Assistant Professor in the Department of Physiology and Cell Biology at The Ohio State University College of Medicine. His research focuses on the molecular mechanisms contributing to the pathophysiologic remodeling of the heart and their role in promoting heart failure. His laboratory investigates the processes underlying adaptive and maladaptive hypertrophic growth of the heart, aiming to identify critical transcriptional and cytoskeletal regulators involved in these mechanisms. The goal of his research is to develop targeted interventions to maintain or restore the adaptive growth stage, thereby preventing heart failure. Dr. Nassal's work evaluates measures of heart contractility, extracellular matrix remodeling and fibrosis, electrical remodeling, and arrhythmia as markers of heart performance. His background includes a PhD from Case Western Reserve University and postdoctoral training at The Ohio State University. His research addresses the rising global burden of heart failure by exploring novel therapeutic approaches to mitigate disease progression.

Research topics

• Internal medicine
• Medicine
• Chemistry
• Endocrinology
• Cancer research
• Biology
• Bioinformatics
• Neuroscience

Selected publications

• Challenges and Opportunities for Therapeutic Targeting of Calmodulin Kinase II in Heart

  Frontiers in Pharmacology · 2020 · 63 citations

  1st authorCorresponding

  /calmodulin-dependent protein kinase II (CaMKII) has received considerable attention over recent years for its central role in maladaptive remodeling and arrhythmias in the setting of chronic disease. However, these basic science discoveries have yet to translate into new therapies for human patients. This review addresses both the promise and barriers to developing translational therapies that target CaMKII signaling to abrogate pathologic remodeling in the setting of chronic disease. Efforts i…

  DOI

• Fibroblast growth factor-inducible 14 mediates macrophage infiltration in heart to promote pressure overload-induced cardiac dysfunction

  Life Sciences · 2020 · 34 citations

  DOI

• Cardiac-Specific Deletion of Scn8a Mitigates Dravet Syndrome-Associated Sudden Death in Adults

  JACC. Clinical electrophysiology · 2024-02-28 · 26 citations

  articleOpen access

  Sudden unexpected death in epilepsy (SUDEP) is a fatal complication experienced by otherwise healthy epilepsy patients. Dravet syndrome (DS) is an inherited epileptic disorder resulting from loss of function of the voltage-gated sodium channel, NaV 1.1, and is associated with particularly high SUDEP risk. Evidence is mounting that NaVs abundant in the brain also occur in the heart, suggesting that the very molecular mechanisms underlying epilepsy could also precipitate cardiac arrhythmias and su…

  PublisherDOI

• Emerging therapeutic targets for cardiac hypertrophy

  Expert Opinion on Therapeutic Targets · 2022-01-02 · 26 citations

  reviewOpen access

  INTRODUCTION: Cardiac hypertrophy is associated with adverse outcomes across cardiovascular disease states. Despite strides over the last three decades in identifying molecular and cellular mechanisms driving hypertrophy, the link between pathophysiological stress stimuli and specific myocyte/heart growth profiles remains unclear. Moreover, the optimal strategy for preventing pathology in the setting of hypertrophy remains controversial. AREAS COVERED: This review discusses molecular mechanisms…

  PublisherOA PDFDOI

• Phospho-ablation of cardiac sodium channel Nav1.5 mitigates susceptibility to atrial fibrillation and improves glucose homeostasis under conditions of diet-induced obesity

  International Journal of Obesity · 2021-01-26 · 21 citations

  articleOpen access

  Abstract Background Atrial fibrillation (AF) is the most common sustained arrhythmia, with growing evidence identifying obesity as an important risk factor for the development of AF. Although defective atrial myocyte excitability due to stress-induced remodeling of ion channels is commonly observed in the setting of AF, little is known about the mechanistic link between obesity and AF. Recent studies have identified increased cardiac late sodium current ( I Na,L ) downstream of calmodulin-depend…

  PublisherOA PDFDOI

Frequent coauthors

• Thomas J. Hund

  The Ohio State University

  62 shared

• Isabelle Deschênes

  The Ohio State University

  38 shared

• Nehal Patel

  36 shared

• Peter J. Mohler

  The Ohio State University

  22 shared

• Xiaoping Wan

  Shanghai First Maternity and Infant Hospital

  20 shared

• Eckhard Ficker

  17 shared

• Amara Greer-Short

  16 shared

• Rebecca Shaheen

  The Ohio State University

  16 shared

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