Jidong Fu

About

Jidong Fu, PhD, is an Associate Professor in the Department of Physiology and Cell Biology at Ohio State College of Medicine. His laboratory focuses on understanding the fundamental mechanisms of cardiac cell fate control and cardiac electrophysiology during heart development, with the aim of developing new therapeutic approaches for cardiac regenerative medicine and anti-arrhythmic therapies. Dr. Fu has over 18 years of experience utilizing mouse and human embryonic stem cells (ESCs) and induced pluripotent stem cells (iPSCs) to study the development of cardiac electrophysiology and automaticity during the differentiation of ESC/iPSC-cardiomyocytes. His research investigates the role of IK1 in cardiac automaticity and anti-arrhythmic therapies, as well as strategies to facilitate the electrophysiological and functional maturation of ESC/iPSC-derived cardiomyocytes to improve their clinical application for cardiac regeneration. Additionally, Dr. Fu's work includes developing epigenetic approaches to directly convert cardiac fibroblasts into induced cardiomyocyte-like cells and exploring the biophysical modulation of microRNAs, revealing novel functions beyond their classical roles that could impact multiple cardiac proteins and diseases.

Research topics

• Biochemistry
• Biophysics
• Chemistry
• Cell biology
• Biology

Selected publications

• Assessment of mitophagy in human iPSC-derived cardiomyocytes

  Autophagy · 2022-02-27 · 27 citations

  articleOpen access

  Defective mitophagy contributes to normal aging and various neurodegenerative and cardiovascular diseases. The newly developed methodologies to visualize and quantify mitophagy allow for additional progress in defining the pathophysiological significance of mitophagy in various model organisms. However, current knowledge regarding mitophagy relevant to human physiology is still limited. Model organisms such as mice might not be optimal models to recapitulate all the key aspects of human disease…

  PublisherOA PDFDOI

• A Heart Failure-Associated SCN5A Splice Variant Leads to a Reduction in Sodium Current Through Coupled-Gating With the Wild-Type Channel

  Frontiers in Physiology · 2021-03-22 · 12 citations

  articleOpen access

  Na v 1.5, encoded by the gene SCN5A , is the predominant voltage-gated sodium channel expressed in the heart. It initiates the cardiac action potential and thus is crucial for normal heart rhythm and function. Dysfunctions in Na v 1.5 have been involved in multiple congenital or acquired cardiac pathological conditions such as Brugada syndrome (BrS), Long QT Syndrome Type 3, and heart failure (HF), all of which can lead to sudden cardiac death (SCD) – one of the leading causes of death worldwide…

  PublisherDOI

• Multilayer control of cardiac electrophysiology by microRNAs

  Journal of Molecular and Cellular Cardiology · 2022-03-02 · 11 citations

  reviewOpen accessSenior authorCorresponding
  PublisherOA PDFDOI

• Inhibition of CREB-CBP Signaling Improves Fibroblast Plasticity for Direct Cardiac Reprogramming

  Cells · 2021-06-22 · 11 citations

  articleOpen accessSenior authorCorresponding

  Direct cardiac reprogramming of fibroblasts into induced cardiomyocytes (iCMs) is a promising approach but remains a challenge in heart regeneration. Efforts have focused on improving the efficiency by understanding fundamental mechanisms. One major challenge is that the plasticity of cultured fibroblast varies batch to batch with unknown mechanisms. Here, we noticed a portion of in vitro cultured fibroblasts have been activated to differentiate into myofibroblasts, marked by the expression of α…

  PublisherOA PDFDOI

• Adipogenic Signaling Promotes Arrhythmia Substrates before Structural Abnormalities in TMEM43 ARVC

  Journal of Personalized Medicine · 2022-10-09 · 10 citations

  articleOpen access

  Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic disorder of desmosomal and structural proteins that is characterized by fibro-fatty infiltrate in the ventricles and fatal arrhythmia that can occur early before significant structural abnormalities. Most ARVC mutations interfere with β-catenin-dependent transcription that enhances adipogenesis; however, the mechanistic pathway to arrhythmogenesis is not clear. We hypothesized that adipogenic conditions play an important role in…

  PublisherOA PDFDOI

Recent grants

• Biophysical Modulation of Cardiac Ion Channels by MicroRNA

  NIH · $4.5M · 2017–2027

Frequent coauthors

• Emre Bektik

  Brigham and Women's Hospital

  56 shared

• Ronald A. Li

  47 shared

• Adrienne T. Dennis

  43 shared

• Isabelle Deschênes

  The Ohio State University

  35 shared

• Kenneth R. Laurita

  MetroHealth

  34 shared

• Deepak Srivastava

  Harcourt Butler Technical University

  31 shared

• Deborah K. Lieu

  29 shared

• Chi‐Wing Kong

  University of Hong Kong

  29 shared

Education

• PhD

  Shanghai Institutes for Biological Sciences

  2006

Similar researchers at Ohio State University

• Sandor Gyorkeh-74
• Vadim Fedorovh-53
• Sissy M. Jhiangh-45