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Updated: Jan 5, 2026

A Flow Cytometry-based Assay for Measuring Mitochondrial Membrane Potential in Cardiac Myocytes After Hypoxia/Reoxygenation
Published on: July 13, 2018
LncRNA SOX2OT Mediates Mitochondrial Dysfunction in Septic Cardiomyopathy
Mengfei Chen1, Yan Guan1, Ao Li2
1Department of Emergency, People's Hospital of Ningxia Hui Autonomous Region (The First Affiliated Hospital of Northwest Minzu University), Ningxia, China.
Long noncoding RNA SOX2 overlapping transcript (SOX2OT) exacerbates mitochondrial dysfunction in septic cardiomyopathy. Inhibiting SOX2OT improves cardiac function and mitochondrial health, offering a potential therapeutic target for this condition.
Area of Science:
- Cardiology
- Molecular Biology
- Genetics
Background:
- Mitochondrial dysfunction is critical in septic cardiomyopathy.
- Long noncoding RNAs (lncRNAs) are implicated in various cardiovascular diseases.
Purpose of the Study:
- To investigate the role of lncRNA SOX2 overlapping transcript (SOX2OT) in septic cardiomyopathy-induced mitochondrial dysfunction.
- To explore the therapeutic potential of targeting SOX2OT.
Main Methods:
- Assessed SOX2OT expression in septic hearts and cardiomyocytes.
- Utilized lncRNA knockdown and overexpression models in mice and cardiomyocytes.
- Evaluated cardiac function, mitochondrial membrane potential, and reactive oxygen species (ROS) production.
Main Results:
- SOX2OT was significantly overexpressed in septic hearts and cardiomyocytes.
- Knockdown of SOX2OT ameliorated cardiac dysfunction and improved mitochondrial membrane potential in lipopolysaccharide (LPS)-induced sepsis.
- SOX2OT overexpression worsened these parameters.
- SOX2OT regulated mitochondrial dysfunction by inhibiting SOX2 expression.
Conclusions:
- SOX2OT promotes mitochondrial dysfunction in septic cardiomyopathy by suppressing SOX2.
- Targeting SOX2OT presents a novel therapeutic strategy for septic cardiomyopathy.
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