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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