Extracellular Nucleic Acids: Emerging Mediators of Myocardial Injury
Presenter: Gausal
Azam Khan
Affiliation: King
Faisal University, Saudi Arabia
Presentation Format:
Keynote Presentation (Virtual)
Tittle: Unveiling
the role of extracellular nucleic acids in hypoxia-induced myocardial injury
🔬 Presentation Overview
🫀 Hypoxia and Cardiovascular Injury
Cardiovascular diseases (CVDs), especially myocardial infarction (MI), are increasingly linked to hypoxia-induced cellular stress rather than infectious causes alone. Hypoxic conditions trigger the release of circulating nucleic acids (CNAs), including extracellular RNA (eRNA) and extracellular DNA (eDNA), which act as inflammatory mediators in cardiovascular pathology.
🧬 Extracellular Nucleic Acids as Inflammatory Triggers
During hypoxia and ischemia-reperfusion injury, necrotic cells release CNAs into circulation. Elevated plasma levels of eRNA and eDNA activate Toll-like receptors (TLRs), initiating sterile inflammation that contributes to vascular damage, coronary artery disease (CAD), and ischemic chest pain.
🔬 Mechanistic Pathway: eRNA–TLR3 Signaling
This study focused on the mechanistic role of eRNA in myocardial injury. Findings demonstrate that hypoxia stimulates eRNA release, which activates Toll-like receptor 3 (TLR3) and downstream caspase-3 signaling. This pathway leads to cardiomyocyte necrosis and increased release of cardiac troponin-T (cTrop-T), a hallmark biomarker of acute myocardial infarction (AMI).
🧪 Key Experimental Findings
·
Hypoxia caused time-dependent increases in
circulating cTrop-T levels
·
RNaseA pre-treatment significantly reduced
myocardial injury markers
·
DNase1 and HMGB1 neutralization showed no
protective effect
·
TLR3 inhibition or gene silencing
markedly decreased cTrop-T release
🩸 Immune Activation and Tissue Damage
The interaction between eRNA and TLR3 promoted leukocyte infiltration and neutrophil activation, exacerbating cardiomyocyte necrosis. These inflammatory processes contributed to myocardial stiffness, impaired cardiac function, and progression toward heart failure
💊 Therapeutic Implications
Targeting extracellular RNA or blocking TLR3 signaling may offer novel
therapeutic strategies to reduce hypoxia-induced myocardial damage. Approaches
such as RNaseA therapy or TLR3 inhibition show promise in limiting sterile
inflammation and protecting cardiac tissue.
🔮
Future Directions in Cardiovascular Therapy
By addressing hypoxia-driven inflammatory pathways, this research opens new avenues for preventing acute myocardial infarction and slowing the development of heart failure in patients with cardiovascular disease.
👩⚕️ About the Speaker
Dr. Gausal Azam Khan, PhD, CSci, FRSM, FRSB, is a Professor of Clinical Nutrition at King Faisal University, Saudi Arabia. His research focuses on insulin resistance, endothelial dysfunction, thrombosis, and hypoxia-driven vascular inflammation. Dr. Khan holds multiple U.S. patents, including a vaccine for Type 2 Diabetes, and has received prestigious distinctions such as Chartered Scientist (CSci), Fellow of the Royal Society of Biology (FRSB), and Fellow of the Royal Society of Medicine (FRSM). With over 100 international publications and extensive global research funding, his work continues to advance understanding of metabolic and vascular pathophysiology under hypoxic stress.
📅 Conference Details
Event: International Conference on Cardiology and
Cardiovascular ScienceDates: March 26–28, 2026
Venue: Singapore & Online
Website: https://cardiology.miconferences.com/
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