Research Interest

Our research focuses on the neuro-cardiovascular interface, exploring how the brain regulates cardiovascular function through molecular and physiological mechanisms. We study how NMDA receptor signaling, neuropeptides, and oxidative stress modulate the brain–heart axis, influencing blood pressure, heart rate, and vascular tone. Dysregulation of these pathways contributes to hypertension and cardiovascular disease.

We also investigate ferroptosis and lipid peroxidation as key processes linking oxidative stress to neuronal and cardiovascular degeneration, providing insight into new therapeutic strategies for hypertension and neurodegenerative disorders.

In addition, we investigate stem cell–based and regenerative therapies, including ADSCs, PBSCs, PRP, and exosomes, for hair regeneration, skin rejuvenation, tissue repair, and joint regeneration, with emphasis on angiogenesis, inflammation, and tissue regeneration.

1. Cardiovascular Pharmacology, Neuropharmacology and Neurophysiology

Cardiovascular Pharmacology: Studies drugs that affect the heart and blood vessels. Focuses on blood pressure regulation, heart rate, vascular tone, and therapies for hypertension, arrhythmia, and heart failure.

Neuropharmacology: Examines how drugs act on the nervous system. Involves neurotransmitters, receptors (like NMDA, GABA, serotonin), and pathways linked to behavior, cognition, and neurological disorders.

Neurophysiology: Explores how neurons and neural circuits function. Covers synaptic transmission, ion channels, electrophysiology, and brain-body regulation (e.g., brain-heart axis).

🔗 Together, these fields explain how the brain controls cardiovascular function, how drugs can modulate this interaction, and how dysfunction leads to disease.

2. Brain–Heart Connection: NMDA Receptors and Cardiovascular Disease

NMDA receptors in the brain play a key role in controlling nerve signals that regulate blood pressure and heart function. When these receptors are overactive or dysfunctional, excessive calcium (Ca²⁺) and sodium (Na⁺) entry into neurons can disturb brain–heart communication. This imbalance may contribute to cardiovascular problems such as hypertension, arrhythmia, and heart disease.

3. The biological activity of NMDA receptors

The biological activity of NMDA receptors at a synapse:

On the left side, the presynaptic terminal, represented as a bulb-like structure containing vesicles filled with neurotransmitters. Some neurotransmitters are shown being released into the synaptic cleft.
On the right side, the postsynaptic membrane is depicted, with an embedded NMDA receptor illustrated in purple.
Neurotransmitters bind to the receptor, leading to the opening of the channel, allowing sodium ions (Na⁺) and calcium ions (Ca²⁺) to flow into the postsynaptic neuron.
The arrows indicate the direction of ion movement through the NMDA receptor channel.
Labels clearly identify the presynaptic neurotransmitters, the NMDA receptor, and the postsynaptic membrane.

Overall, the image visually explains how NMDA receptor activation facilitates ion entry, which is essential for synaptic signaling and plasticity.

4. The Pharmacological Effects of Neuropeptides Linked to NMDA Receptor Activity, Brain–Heart Axis, and Cardiovascular Disease

Neuropeptides are brain signaling molecules that modulate neuronal activity and interact with receptors to influence communication between the brain and body. By affecting systems such as the NMDA receptor pathway, they play important roles in regulating cardiovascular function, stress responses, and neuroprotection.

Neuropeptides are also chemical messengers that regulate brain function and influence cardiovascular health. By modulating receptors at synapses, they affect neural activity, blood pressure, heart rhythm, and stress responses—making them important targets in both neuroscience and cardiovascular medicine.

5. The pathophysiological mechanisms of hypertension. (link between neuropeptides, NMDA receptor activity, and hypertension)

The image explains how neuropeptides regulate NMDA receptor activity in the brain, influencing cardiovascular health and the development of hypertension.

Brain – Neuropeptides are released from neurons in the central nervous system (CNS).

Synapse – These neuropeptides act on the NMDA receptor, which controls the flow of ions such as calcium (Ca²⁺) and sodium (Na⁺) into neurons.

NMDA Receptor Activity – Overactivation or dysregulation leads to altered neuronal signaling that can affect autonomic control.

Heart and Blood Vessels – This abnormal signaling contributes to cardiovascular dysfunction, including hypertension (high blood pressure).

6. The central mechanisms underlying hypertension, focusing on central circulatory regulation and sympathetic activation

🔹 Main Pathways in the Brain

PVN (Paraventricular Nucleus): Receives excitatory inputs from angiotensin II and other stimuli. Sends projections to RVLM and other brainstem nuclei.

RVLM (Rostral Ventrolateral Medulla): The key region controlling sympathetic outflow. Inputs: excitatory (e.g., glutamate, angiotensin II) and inhibitory (e.g., GABA). Modulated by nitric oxide (inhibitory, vasodilatory) and oxidative stress (excitatory, harmful). When oxidative stress dominates, sympathetic activation increases.

CVLM (Caudal Ventrolateral Medulla): Provides inhibitory input (mainly via GABA) to RVLM, helping to balance excitatory drive.

NTS (Nucleus Tractus Solitarius): Integrates signals from baroreceptors (blood pressure sensors) and circulating angiotensin II, sending excitatory and inhibitory signals to RVLM and PVN.

🔹 Sympathetic Outflow: All these integrated signals converge to regulate sympathetic outflow.

Increased excitatory drive (glutamate, angiotensin II, oxidative stress) → higher sympathetic activation.
Decreased inhibitory drive (GABA, nitric oxide) → loss of balance, further enhancing sympathetic activity.

🔹 Link to Hypertension

Excess sympathetic activation → vasoconstriction, increased heart rate, renal effects → sustained hypertension.
Thus, hypertension emerges when excitatory inputs and oxidative stress outweigh inhibitory regulation.

7. Ferroptosis exploring its link to cardiovascular and neurodegenerative diseases.

The role of lipid peroxidation and ferroptosis in Alzheimer’s disease (AD) neurodegeneration.

Triggers of Lipid Peroxidation:

Polyunsaturated fatty acids (PUFAs): Highly prone to oxidative damage.

Labile iron: Catalyzes lipid peroxidation via Fenton reactions.

Decreased GSH (Glutathione): Reduces antioxidant capacity.

Reduced antioxidant defenses: Can be caused by stroke, traumatic brain injury (TBI), etc.

Lipid Peroxidation: All these factors converge to promote lipid peroxidation, which damages cell membranes.

Ferroptosis: Lipid peroxidation leads to ferroptosis, a form of regulated cell death dependent on iron and oxidative stress.

Neurodegeneration in AD: Ferroptosis contributes to neuronal loss and neurodegeneration in Alzheimer’s disease.

Protective Interventions: Iron chelators (e.g., deferiprone) and antioxidants (e.g., N-acetylcysteine, CuATSM, vitamin E) can inhibit lipid peroxidation and potentially reduce ferroptosis-mediated damage.

👉 In summary: Oxidative stress, iron overload, and reduced antioxidant defenses drive lipid peroxidation → ferroptosis → neurodegeneration in AD.

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