Michael Tranter

About

Michael Tranter, PhD, is an Associate Professor in the Department of Molecular Medicine and Therapeutics at Ohio State College of Medicine. His research focuses on understanding the molecular mechanisms of post-transcriptional gene regulation that drive cardiometabolic diseases. His lab has demonstrated a functional role for the RNA binding protein HuR in the pathophysiology of cardiac remodeling, acting in both myocytes and fibroblasts. Additionally, his work has contributed to the field of adipose tissue biology, particularly in understanding how disruptions in adipose tissue homeostasis impact cardiac physiology. Dr. Tranter's research employs multi-disciplinary, mechanism-focused translational systems physiology approaches using both mouse and human tissues. His ongoing projects include studying pathological left ventricular cardiac hypertrophy and fibrosis leading to heart failure, calcium-mediated thermogenic metabolism in brown adipocytes, and adipose tissue-mediated endocrine effects on cardiac physiology. He earned his PhD in Molecular Pharmacology from the University of Cincinnati, College of Medicine, and his BS in Molecular Biology from Rose-Hulman Institute of Technology.

Research topics

• Internal medicine
• Endocrinology
• Medicine
• Biology
• Genetics
• Pharmacology
• Immunology
• Biochemistry
• Cardiology

Selected publications

• <scp>HuR</scp> inhibition reduces post‐ischemic cardiac remodeling by dampening myocyte‐dependent inflammatory gene expression and the innate immune response

  The FASEB Journal · 2025-03-14 · 6 citations

  articleOpen accessSenior authorCorresponding

  The RNA-binding protein human antigen R (HuR) has been shown to reduce cardiac remodeling following both myocardial infarction and cardiac pressure overload, but the full extent of the HuR-dependent mechanisms within cells of the myocardium has yet to be elucidated. Wild-type mice were subjected to 30 min of cardiac ischemia (via LAD occlusion) and treated with a novel small molecule inhibitor of HuR at the time of reperfusion, followed by direct in vivo assessment of cardiac structure and funct…

  PublisherOA PDFDOI

• RNA binding proteins as mediators of pathological cardiac remodeling

  Frontiers in Cell and Developmental Biology · 2024-05-16 · 4 citations

  reviewOpen accessSenior authorCorresponding

  RNA binding proteins (RBPs) play a central in the post-transcriptional regulation of gene expression, which can account for up to 50% of all variations in protein expression within a cell. Following their binding to target RNAs, RBPs most typically confer changes in gene expression through modulation of alternative spicing, RNA stabilization/degradation, or ribosome loading/translation rate. All of these post-transcriptional regulatory processes have been shown to play a functional role in patho…

  PublisherOA PDFDOI

• Cardiac macrophages and fibroblasts: A synergistic partnership without cellular transition

  Journal of Molecular and Cellular Cardiology · 2024-09-19 · 2 citations

  editorialOpen access
  PublisherOA PDFDOI

• <i>MCM2</i> mediates post-MI cardioprotection by promoting the pro-angiogenic cardiosome signaling

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-12-17 · 1 citations

  preprintOpen access

  Abstract Background In the past decade, induced cardiac rejuvenation has emerged as a leading approach to repair cardiac injury. Recent studies demonstrate that promoting cell cycle reentry in adult cardiomyocytes (CM) enhances cardiac rejuvenation by influencing paracrine signaling. We previously demonstrated that the inhibition of two cell cycle inhibitors, Retinoblastoma 1 (Rb1) and Meis homeobox 2 (Meis2), in the adult CM enhances angiogenesis and cardiac function following ischemic injury,…

  PublisherOA PDFDOI

• PAR2 (Protease-Activated Receptor 2) Deficiency Attenuates Atherosclerosis in Mice

  UNC Libraries · 2026-03-20

  articleOpen access

  OBJECTIVE: PAR2 (protease-activated receptor 2)-dependent signaling results in augmented inflammation and has been implicated in the pathogenesis of several autoimmune conditions. The objective of this study was to determine the effect of PAR2 deficiency on the development of atherosclerosis. APPROACH AND RESULTS: PAR2 mRNA and protein expression is increased in human carotid artery and mouse aortic arch atheroma versus control carotid and aortic arch arteries, respectively. To determine the eff…

  PublisherDOI

Recent grants

• NIH Grant R01HL132111

  NIH · $1.8M · 2022

Frequent coauthors

• Sarah Anthony

  The Ohio State University

  45 shared

• Xiaoping Ren

  Guangxi University of Chinese Medicine

  22 shared

• Samuel Slone

  University of Cincinnati Medical Center

  22 shared

• Jack Rubinstein

  University of Cincinnati Medical Center

  22 shared

• A. Phillip Owens

  University of Cincinnati Medical Center

  21 shared

• Michelle L. Nieman

  University of Cincinnati Medical Center

  18 shared

• Adrienne Guarnieri

  University of Cincinnati Medical Center

  18 shared

• W. Keith Jones

  Loyola University Chicago

  17 shared

Education

• Post-Doctoral Fellowship, Pharmacology

  University of Cincinnati College of Medicine

  2012

• Ph.D., Molecular, Cellular, and Biochemical Pharmacology

  University of Cincinnati College of Medicine

  2010

• B.S.

  Rose Hulman Institute of Technology

  2004

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