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Professor Nipon Chattipakorn and Professor Siriporn C Chattipakorn: Shares Study Insights at CVMD Research Seminar

Seminar Details

Date:	23 February, Monday
Time:	4:00 PM to 5:00 PM
Venue:	Meeting room 7C, Level 7
Speaker 1:	Professor Nipon Chattipakorn Director, Cardiac Electrophysiology Research and Training Centre (CERT), Faculty of Medicine, Chiang Mai University
Talk Title:	*"Acute and Chronic Mitochondrial Dynamic Modulations in Cardiac Ischemia-reperfusion Injury, Myocardial Infarction, and Cardiotoxicity”*
Synopsis:
Alterations in mitochondrial dynamics play a crucial role in the pathophysiological processes of the heart, including ischemia-reperfusion injury, myocardial infarction, and chemotherapy-induced cardiotoxicity. Since an imbalance in mitochondrial dynamics in the heart is one of the key contributors to left ventricular dysfunction in these conditions, we demonstrated that maintaining this balance offers potential therapeutic benefits. Targeting mitochondrial dynamics may help mitigate these pathologies and ultimately improve cardiac function.
Speaker 2:	Professor Siriporn Chattipakorn Neuroscience and Oral Biology Neurophysiology Unit, Cardiac Electrophysiology Research and Training Center (CERT), Faculty of Medicine, Chiang Mai University
Talk Title 2:	*“Pathophysiological Changes in The Brain Following Myocardial Infarction”*
Synopsis
Myocardial infarction (MI) leads to heart failure–associated cognitive impairment through reduced cerebral perfusion, oxidative stress, inflammation, mitochondrial dysfunction, dendritic spine loss, and apoptosis. Experimental studies show that MI rats develop cardiac dysfunction, blood–brain barrier disruption, and cognitive decline. Chronic treatment with the apoptosis inhibitor Z-vad improved cardiac and cognitive function, restored dendritic spine density, reduced oxidative stress and mitochondrial dysfunction, and enhanced mitophagy and neurogenesis, with greater neuroprotection than enalapril. In contrast, sodium–glucose co-transporter 2 inhibitors (SGLT2i) improved cardiac function and brain glutamate levels and partially improved mitochondrial function but failed to restore cognitive function or synaptic plasticity. These findings highlight brain apoptosis as a key therapeutic target for HF-related cognitive impairment.

Date and Time

23 Feb 2026 @ 16:00 - 23 Feb 2026 @ 17:00