Fang Zheng
Professor
Also affiliated: State University of New York (2003); Emory University (1996–2003); Chiba University (2003); University of Freiburg (2011); National University of Singapore (2003); Heidelberg University (2012); State Administration of Traditional Chinese Medicine of the People's Republic of China (2018); University of Arkansas Medical Center (2017); Wuhan University (2017); Wuhan Dongxihu District People Hospital (2015); Universitätsklinikum des Saarlandes (2011); National Institute of Environmental Health Sciences (2011–2012); Shanghai University of Traditional Chinese Medicine (2018–2023); National Center for Gene Research (2015); Wuhan Donghu University (2015); Zhongnan Hospital of Wuhan University (2017); National Neuroscience Institute (2003); Huangshi Central Hospital (2018); Health and Human Development (2HD) Research Network (2011); Baoding People's Hospital (2017); First Affiliated Hospital Zhejiang University (2015); Huazhong University of Science and Technology (2011–2016); The University of Texas Medical Branch at Galveston (1991–1995); The University of Tokyo (2009); Saarland University (2011–2012)
Faculty Researcher
Pharmacology & Toxicology, College of Medicine
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Fang Zheng investigates the roles of transient receptor potential (TRP) channels in neurological and vascular functions. His research group studies the TRPC3 channel's involvement in hippocampal hyperexcitability and neuronal cell death, as well as its function in neurovascular coupling, particularly in relation to endothelial NPYR1-TRPC3-ET1 signaling.
Dr. Zheng's work also examines the pharmacological distinctions between homomeric and heteromeric TRP channels, specifically TRPC4 and TRPC1/4 channels in lateral septal neurons. His laboratory has explored the effects of venlafaxine on gut microbiota in a mouse model of chronic unpredictable mild stress-induced depression. Additional research interests include the self-assembly and cellular calcium transport capabilities of vitamin D3-mediated peptides and the reliability of DRAM systems through error correction codes.
With an h-index of 23 and over 2,400 citations from 58 publications, Dr. Zheng has received federal funding, including a $372,745 NIH/NINDS grant for his work on neurovascular coupling. He collaborates with researchers at the University of Arkansas for Medical Sciences and the University of Arkansas at Fayetteville.
Metrics
- h-index: 23
- Publications: 58
- Citations: 2,503
Selected Publications
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Increased luminal pressure in brain capillaries drives TRPC3-dependent depolarization and constriction of transitional pericytes (2025)
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Investigating Contributions of Canonical Transient Receptor Potential Channel 3 to Hippocampal Hyperexcitability and Seizure-Induced Neuronal Cell Death (2024)
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Increased Susceptibility to Pilocarpine-Induced Status Epilepticus and Reduced Latency in TRPC1/4 Double Knockout Mice (2023)
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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)
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Canonical Transient Receptor Potential Channel 3 Contributes to Cerebral Blood Flow Changes Associated with Cortical Spreading Depression in Mice (2023)
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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)
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Canonical Transient Receptor Potential Channels as Novel Targets for Antiepileptic Drugs (2022)
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Leptin Activates Trpm7 Channels in the Carotid Body As a Mechanism of Obesity-Related Hypertension (2019)
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Elucidating the Involvement of Endothelial TRPC3 Channels in Neurovascular Coupling During Status Epilepticus (2018)
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TRPC Channels and Epilepsy (2017)
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<scp>TRPC</scp>3 channels play a critical role in the theta component of pilocarpine‐induced status epilepticus in mice (2016)
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Pilocarpine-induced status epilepticus in mice: A comparison of spectral analysis of electroencephalogram and behavioral grading using the Racine scale (2015)
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The Role of Canonical Transient Receptor Potential Channels in Seizure and Excitotoxicity (2014)
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Critical role of canonical transient receptor potential channel 7 in initiation of seizures (2014)
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Genetic deletion of the TRPC3 channel blunts the development of angiotensin II‐induced hypertension in mice (2013)
Federal Grants 1 $372,745 total
The Role of the Endothelial NPYR1-TRPC3-ET1 Signaling Axis in Neurovascular Coupling Dysfunction
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
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- 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
- ZINC-DEPENDENT APPARENT DESENSITIZATION OF NMDA RECEPTOR NIH Principal Investigator
- Neuroscience Research Center Core Facility at UAMS NIH Co-Investigator
- MODULATION OF NMDA RECEPTORS BY TYROSINE KINASES NIH Principal Investigator
- Canonical Transient Receptor Potential Channels and Excitotoxicity NIH Principal Investigator
- METABOTROPIC GLUTAMATE RECEPTORS AND EXCITOTOXICITY NIH Principal Investigator
Collaboration Network
Top Collaborators
- 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
- Investigating Contributions of Canonical Transient Receptor Potential Channel 3 to Hippocampal Hyperexcitability and Seizure-Induced Neuronal Cell Death
- Increased Susceptibility to Pilocarpine-Induced Status Epilepticus and Reduced Latency in TRPC1/4 Double Knockout Mice
- 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
- Investigating Contributions of Canonical Transient Receptor Potential Channel 3 to Hippocampal Hyperexcitability and Seizure-Induced Neuronal Cell Death
- Increased Susceptibility to Pilocarpine-Induced Status Epilepticus and Reduced Latency in TRPC1/4 Double Knockout Mice
- 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
- 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
- Investigating Contributions of Canonical Transient Receptor Potential Channel 3 to Hippocampal Hyperexcitability and Seizure-Induced Neuronal Cell Death
- Increased luminal pressure in brain capillaries drives TRPC3-dependent depolarization and constriction of transitional pericytes
- Increased luminal pressure in brain capillaries drives TRPC3-dependent depolarization and constriction of transitional pericytes
- Increased luminal pressure in brain capillaries drives TRPC3-dependent depolarization and constriction of transitional pericytes
- Increased luminal pressure in brain capillaries drives TRPC3-dependent depolarization and constriction of transitional pericytes
- Increased luminal pressure in brain capillaries drives TRPC3-dependent depolarization and constriction of transitional pericytes
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