J
Jonathan D. Hoang Data-verified
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
Postdoctoral Fellow
postdoc
10 h-index
35 pubs
490 cited
Research Areas
Links
Biography and Research Information
OverviewAI-generated summary
Jonathan D. Hoang's research investigates the complex interplay between the nervous and cardiovascular systems, particularly in the context of disease states like myocardial infarction and type 2 diabetes. His work has explored how interventions such as vagal nerve stimulation can mitigate adverse cardiac events, including proarrhythmic effects caused by sympathetic activation. Hoang has also studied the role of specific neurotransmitters, like neuropeptide Y, in modulating cardiac function and the impact of conditions like diabetes on insulin-secreting cells and cholesterol homeostasis. His research utilizes animal models, including swine, and examines molecular mechanisms, such as the activation of beta-adrenergic receptors and Y2-receptor blockade. Hoang's publication record includes work on gene delivery techniques targeting the brain and the pathological autonomic remodeling that occurs after chronic myocardial infarction.
Metrics
- h-index: 10
- Publications: 35
- Citations: 490
Selected Publications
-
Overexpression and biophysical and functional characterization of a recombinant FGF21 (2025)
-
Characterizing fibroblast growth factor 21 through biophysical methods (2024)
Collaboration Network
Top Collaborators
Marmar Vaseghi
Los Angeles Medical Center (US)
14 shared publications
- Myocardial infarction reduces cardiac nociceptive neurotransmission through the vagal ganglia
- Proarrhythmic Effects of Sympathetic Activation Are Mitigated by Vagal Nerve Stimulation in Infarcted Hearts
- Circulating noradrenaline leads to release of neuropeptide Y from cardiac sympathetic nerve terminals via activation of β‐adrenergic receptors
- Thoracic epidural blockade after myocardial infarction benefits from anti-arrhythmic pathways mediated in part by parasympathetic modulation
- BS-469619-001 SPINAL AFFERENT DENERVATION AMELIORATES PATHOLOGICAL AUTONOMIC REMODELING AND REDUCES VENTRICULAR ARRHYTHMIAS AFTER CHRONIC MYOCARDIAL INFARCTION
Showing 5 of 14 shared publications
Zulfiqar A. Lokhandwala
Texas Cardiac Arrhythmia (US)
7 shared publications
- Myocardial infarction reduces cardiac nociceptive neurotransmission through the vagal ganglia
- Thoracic epidural blockade after myocardial infarction benefits from anti-arrhythmic pathways mediated in part by parasympathetic modulation
- BS-469619-001 SPINAL AFFERENT DENERVATION AMELIORATES PATHOLOGICAL AUTONOMIC REMODELING AND REDUCES VENTRICULAR ARRHYTHMIAS AFTER CHRONIC MYOCARDIAL INFARCTION
- Abstract 11494: Electrophysiological Effects of Sympathoexcitation are Mitigated by Blockade of Neuropeptide Y Y2 Receptors on Cardiac Parasympathetic Nerve Terminals
- Sympathetic nociceptive afferent signaling drives the chronic structural and functional autonomic remodeling after myocardial infarction
Showing 5 of 7 shared publications
Neil Jani
University of California, Los Angeles (US)
7 shared publications
- Circulating noradrenaline leads to release of neuropeptide Y from cardiac sympathetic nerve terminals via activation of β‐adrenergic receptors
- BS-469619-001 SPINAL AFFERENT DENERVATION AMELIORATES PATHOLOGICAL AUTONOMIC REMODELING AND REDUCES VENTRICULAR ARRHYTHMIAS AFTER CHRONIC MYOCARDIAL INFARCTION
- PO-01-173 VAGAL NERVE STIMULATION REDUCES INTERSTITIAL VENTRICULAR NEUROPEPTIDE Y RELEASE VIA ACTIVATION OF PRESYNAPTIC SYMPATHETIC MUSCARINIC RECEPTORS
- Sympathetic nociceptive afferent signaling drives the chronic structural and functional autonomic remodeling after myocardial infarction
- NEUROPEPTIDE Y RECEPTOR INHIBITOR ENHANCES EFFECTS OF VAGAL NERVE STIMULATION AND REDUCES EFFECTS OF SYMPATHETIC ACTIVATION: ASSESSMENTS USING REAL-TIME ELECTROPHYSIOLOGICAL AND MYOCARDIAL NEUROPEPTIDE MEASUREMENTS
Showing 5 of 7 shared publications
Maryam Emamimeybodi
Los Angeles Medical Center (US)
7 shared publications
- BS-469619-001 SPINAL AFFERENT DENERVATION AMELIORATES PATHOLOGICAL AUTONOMIC REMODELING AND REDUCES VENTRICULAR ARRHYTHMIAS AFTER CHRONIC MYOCARDIAL INFARCTION
- Sympathovagal crosstalk: Y2-receptor blockade enhances vagal effects which in turn reduce NPY levels via muscarinic receptor activation
- Abstract 11494: Electrophysiological Effects of Sympathoexcitation are Mitigated by Blockade of Neuropeptide Y Y2 Receptors on Cardiac Parasympathetic Nerve Terminals
- Sympathetic nociceptive afferent signaling drives the chronic structural and functional autonomic remodeling after myocardial infarction
- NEUROPEPTIDE Y RECEPTOR INHIBITOR ENHANCES EFFECTS OF VAGAL NERVE STIMULATION AND REDUCES EFFECTS OF SYMPATHETIC ACTIVATION: ASSESSMENTS USING REAL-TIME ELECTROPHYSIOLOGICAL AND MYOCARDIAL NEUROPEPTIDE MEASUREMENTS
Showing 5 of 7 shared publications
Christopher A. Chan
University of California, Los Angeles (US)
6 shared publications
- Scalable and reversible axonal neuromodulation of the sympathetic chain for cardiac control
- Proarrhythmic Effects of Sympathetic Activation Are Mitigated by Vagal Nerve Stimulation in Infarcted Hearts
- Thoracic epidural blockade after myocardial infarction benefits from anti-arrhythmic pathways mediated in part by parasympathetic modulation
- Abstract 11494: Electrophysiological Effects of Sympathoexcitation are Mitigated by Blockade of Neuropeptide Y Y2 Receptors on Cardiac Parasympathetic Nerve Terminals
- Sympathetic nociceptive afferent signaling drives the chronic structural and functional autonomic remodeling after myocardial infarction
Showing 5 of 6 shared publications
Viviana Gradinaru
6 shared publications
- AAVs targeting human carbonic anhydrase IV enhance gene delivery to the brain
- The gut microbiome promotes mitochondrial respiration in the brain of a Parkinson’s disease mouse model
- Programmable self-assembling system to model intracellular protein aggregation and decode neurodegenerative diseases
- AAVs Targeting Human Carbonic Anhydrase IV Enhance Gene Delivery to the Brain
- Programmable Self-Assembling System to Model Intracellular Protein Aggregation and Decode Neurodegenerative Diseases
Showing 5 of 6 shared publications
Mohammed Amer Swid
University of California, Los Angeles (US)
5 shared publications
- Myocardial infarction reduces cardiac nociceptive neurotransmission through the vagal ganglia
- Scalable and reversible axonal neuromodulation of the sympathetic chain for cardiac control
- Thoracic epidural blockade after myocardial infarction benefits from anti-arrhythmic pathways mediated in part by parasympathetic modulation
- Abstract 11494: Electrophysiological Effects of Sympathoexcitation are Mitigated by Blockade of Neuropeptide Y Y2 Receptors on Cardiac Parasympathetic Nerve Terminals
- Abstract 10597: Epidural Sympathetic Afferent Blockade by Resiniferatoxin Reverses Vagal Dysfunction Following Myocardial Infarction
Corey Smith
Case Western Reserve University (US)
4 shared publications
- Scalable and reversible axonal neuromodulation of the sympathetic chain for cardiac control
- Circulating noradrenaline leads to release of neuropeptide Y from cardiac sympathetic nerve terminals via activation of β‐adrenergic receptors
- Sympathovagal crosstalk: Y2-receptor blockade enhances vagal effects which in turn reduce NPY levels via muscarinic receptor activation
- PO-01-173 VAGAL NERVE STIMULATION REDUCES INTERSTITIAL VENTRICULAR NEUROPEPTIDE Y RELEASE VIA ACTIVATION OF PRESYNAPTIC SYMPATHETIC MUSCARINIC RECEPTORS
Neil R Jani
Los Angeles Medical Center (US)
4 shared publications
- Thoracic epidural blockade after myocardial infarction benefits from anti-arrhythmic pathways mediated in part by parasympathetic modulation
- Sympathovagal crosstalk: Y2-receptor blockade enhances vagal effects which in turn reduce NPY levels via muscarinic receptor activation
- Abstract 11494: Electrophysiological Effects of Sympathoexcitation are Mitigated by Blockade of Neuropeptide Y Y2 Receptors on Cardiac Parasympathetic Nerve Terminals
- Abstract 10597: Epidural Sympathetic Afferent Blockade by Resiniferatoxin Reverses Vagal Dysfunction Following Myocardial Infarction
Christopher T. Chan
University of California, Los Angeles (US)
4 shared publications
- BS-469619-001 SPINAL AFFERENT DENERVATION AMELIORATES PATHOLOGICAL AUTONOMIC REMODELING AND REDUCES VENTRICULAR ARRHYTHMIAS AFTER CHRONIC MYOCARDIAL INFARCTION
- Pro-Arrhythmic Effects of Sympathetic Activation are Mitigated by Vagal Nerve Stimulation in Infarcted Hearts
- NEUROPEPTIDE Y RECEPTOR INHIBITOR ENHANCES EFFECTS OF VAGAL NERVE STIMULATION AND REDUCES EFFECTS OF SYMPATHETIC ACTIVATION: ASSESSMENTS USING REAL-TIME ELECTROPHYSIOLOGICAL AND MYOCARDIAL NEUROPEPTIDE MEASUREMENTS
- Sympathetic nociceptive afferent signaling drives the chronic structural and functional autonomic remodeling after myocardial infarction
Yujie Fan
California Institute of Technology (US)
4 shared publications
- AAVs targeting human carbonic anhydrase IV enhance gene delivery to the brain
- Programmable self-assembling system to model intracellular protein aggregation and decode neurodegenerative diseases
- AAVs Targeting Human Carbonic Anhydrase IV Enhance Gene Delivery to the Brain
- Programmable Self-Assembling System to Model Intracellular Protein Aggregation and Decode Neurodegenerative Diseases
Changfan Lin
California Institute of Technology (US)
4 shared publications
- AAVs targeting human carbonic anhydrase IV enhance gene delivery to the brain
- Programmable self-assembling system to model intracellular protein aggregation and decode neurodegenerative diseases
- AAVs Targeting Human Carbonic Anhydrase IV Enhance Gene Delivery to the Brain
- Programmable Self-Assembling System to Model Intracellular Protein Aggregation and Decode Neurodegenerative Diseases
Robert L. Lux
University of Utah (US)
3 shared publications
- Proarrhythmic Effects of Sympathetic Activation Are Mitigated by Vagal Nerve Stimulation in Infarcted Hearts
- Thoracic epidural blockade after myocardial infarction benefits from anti-arrhythmic pathways mediated in part by parasympathetic modulation
- Pro-Arrhythmic Effects of Sympathetic Activation are Mitigated by Vagal Nerve Stimulation in Infarcted Hearts
Valerie Van Weperen
UCLA Health (US)
3 shared publications
- Sympathetic nociceptive afferent signaling drives the chronic structural and functional autonomic remodeling after myocardial infarction
- NEUROPEPTIDE Y RECEPTOR INHIBITOR ENHANCES EFFECTS OF VAGAL NERVE STIMULATION AND REDUCES EFFECTS OF SYMPATHETIC ACTIVATION: ASSESSMENTS USING REAL-TIME ELECTROPHYSIOLOGICAL AND MYOCARDIAL NEUROPEPTIDE MEASUREMENTS
- CIRCULATING NOREPINEPHRINE LEADS TO RELEASE OF NEUROPEPTIDE Y AT CARDIAC SYMPATHETIC NERVE TERMINALS
Sartaj Bal
Los Angeles Medical Center (US)
3 shared publications
- Sympathovagal crosstalk: Y2-receptor blockade enhances vagal effects which in turn reduce NPY levels via muscarinic receptor activation
- NEUROPEPTIDE Y RECEPTOR INHIBITOR ENHANCES EFFECTS OF VAGAL NERVE STIMULATION AND REDUCES EFFECTS OF SYMPATHETIC ACTIVATION: ASSESSMENTS USING REAL-TIME ELECTROPHYSIOLOGICAL AND MYOCARDIAL NEUROPEPTIDE MEASUREMENTS
- CIRCULATING NOREPINEPHRINE LEADS TO RELEASE OF NEUROPEPTIDE Y AT CARDIAC SYMPATHETIC NERVE TERMINALS
Similar Researchers
Based on overlapping research topics
Murat M.D. Gokden
University of Arkansas for Medical Sciences
Metabolism and Genetic Disorders
Disease Mechanisms Research
Animal Behavior and Welfare Studies
Emily D. Sprick
University of Arkansas for Medical Sciences
Cardiovascular Function and Risk Factors
Metabolism and Genetic Disorders
Disease Mechanisms Research
Swastika Tandon
University of Arkansas at Fayetteville
Cardiovascular Function and Risk Factors
Metabolism and Genetic Disorders
Disease Mechanisms Research
Anusha Bhattacharyya
University of Arkansas for Medical Sciences
Cardiovascular Function and Risk Factors
Metabolism and Genetic Disorders
Disease Mechanisms Research
Hannah Campbell
University of Central Arkansas
Cardiovascular Function and Risk Factors
Metabolism and Genetic Disorders
Disease Mechanisms Research
Claudia C.S. Chini
University of Arkansas for Medical Sciences
Cardiovascular Function and Risk Factors
Metabolism and Genetic Disorders
Neuroscience and Neural Engineering