Fang Zheng

Federal Grant PI High Impact

Professor

Last publication 2025 Last refreshed 2026-05-22

faculty

Pharmacology & Toxicology, College of Medicine

23 h-index 58 pubs 2,459 cited

Biography and Research Information

OverviewAI-generated summary

Fang Zheng's research investigates the role of ion channels, particularly Transient Receptor Potential Canonical (TRPC) channels, in neurological and physiological processes. His work has explored the function of TRPC3 channels in hippocampal hyperexcitability and seizure-induced neuronal death, as well as their involvement in neurovascular coupling and brain capillary function. Zheng has also examined the pharmacological differences between native and heteromeric TRPC4 channels in specific neuronal populations.

His research extends to the impact of pharmacological agents and physiological conditions on the nervous system. This includes studies on the alteration of gut microbiota in depression models treated with venlafaxine and the effects of synthetic cannabinoid receptor agonists on electroencephalographic seizures. Zheng also has an interest in nutritional interventions, evidenced by his work on Vitamin D3 mediated peptide-calcium chelate self-assembly and its effects on cellular calcium transport.

Zheng holds a Professor position in Pharmacology & Toxicology at the University of Arkansas for Medical Sciences. His scholarly output includes 63 publications, with an h-index of 23 and over 2,400 citations. He has received federal funding from the NIH/National Institute of Neurological Disorders and Stroke for his research on the TRPC3 signaling axis in neurovascular coupling dysfunction. Zheng actively collaborates with researchers at his institution, including Kevin D. Phelan and U Thaung Shwe.

Metrics

  • h-index: 23
  • Publications: 58
  • Citations: 2,459

Selected Publications

  • Increased luminal pressure in brain capillaries drives TRPC3-dependent depolarization and constriction of transitional pericytes (2025)
    9 citations DOI OpenAlex
  • Investigating Contributions of Canonical Transient Receptor Potential Channel 3 to Hippocampal Hyperexcitability and Seizure-Induced Neuronal Cell Death (2024)
    5 citations DOI OpenAlex
  • Increased Susceptibility to Pilocarpine-Induced Status Epilepticus and Reduced Latency in TRPC1/4 Double Knockout Mice (2023)
  • Pharmacological Differences between Native Homomeric Transient Receptor Potential Canonical Type 4 Channels and Heteromeric Transient Receptor Potential Canonical Type 1/4 Channels in Lateral Septal Neurons (2023)
    5 citations DOI OpenAlex
  • Canonical Transient Receptor Potential Channel 3 Contributes to Cerebral Blood Flow Changes Associated with Cortical Spreading Depression in Mice (2023)
    2 citations DOI OpenAlex
  • Convulsant doses of abused synthetic cannabinoid receptor agonists AB-PINACA, 5F-AB-PINACA, 5F-ADB-PINACA and JWH-018 do not elicit electroencephalographic (EEG) seizures in male mice (2022)
    4 citations DOI OpenAlex
  • Canonical Transient Receptor Potential Channels as Novel Targets for Antiepileptic Drugs (2022)
    4 citations DOI OpenAlex

View all publications on OpenAlex →

Federal Grants 1 $372,745 total

NIH/National Institute of Neurological Disorders and Stroke Contact PI Mar 2023 - Feb 2028

The Role of the Endothelial NPYR1-TRPC3-ET1 Signaling Axis in Neurovascular Coupling Dysfunction

National Institute of Neurological Disorders and Stroke $372,745 R01

Research Interests

I have a long-standing interest in the pathophysiology of epilepsy and stroke. Initially trained as a channel biophysicist, I have also acquired experience and knowledge in molecular biology, biochemistry and pharmacology over the years. This allows me to adopt a multidisciplinary approach in my research. I have a equally long-standing interest in the functional roles of metabotropic glutamate receptor (mGluR), and this interest has led to my recent focus on transient receptor potential (TRPC) channels for the last 6 years. We have demonstrated the unique roles of various TRPC family members in seizure and excitotoxicity.

Grants & Funding

  • The role of TRPC3 channels in neurovascular coupling and peri-infarct depression UAMS College of Medicine Principal Investigator
  • The role of TRPC3 channels in periinfarct depression and stroke UAMS Stroke - Foundation Principal Investigator
  • The Role of Endothelial TRPC3 Channels in Neurovascular Coupling NIH Principal Investigator
  • The role of TRPC3 channels in neurovascular coupling and peri-infarct depression UAMS College of Medicine Principal Investigator
  • ZINC-DEPENDENT APPARENT DESENSITIZATION OF NMDA RECEPTOR NIH Principal Investigator
  • Neuroscience Research Center Core Facility at UAMS NIH Co-Investigator
  • The role of the endothelial NPYR1-TRPC3-ET1 signaling axis in neurovascular coupling dysfunction NIH Principal Investigator
  • MODULATION OF NMDA RECEPTORS BY TYROSINE KINASES NIH Principal Investigator

Collaboration Network

60 Collaborators 16 Institutions 2 Countries

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