Scholarlink

<p>Acute coronary syndrome (ACS) is a significant contributor to cardiovascular mortality. Research has indicated that CA125 levels are linked to cardiovascular disease. This study aimed to explore the role of CA125 in ACS and its underlying mechanism. A retrospective study was conducted involving 34 healthy volunteers and 46 patients diagnosed with ACS. Clinical characteristics and CA125 expression were recorded and detected. Bioinformatics analysis was performed to identify miRNAs that regulate CA125. HL-1 cardiac muscle cells were subjected to oxygen–glucose deprivation/reoxygenation (OGD/R) to investigate the role of CA125 in myocardial injury. An ACS mice model was constructed to further explore the role of CA125 on ACS. The levels of serum creatinine, blood urea nitrogen, uric acid, high-sensitivity C-reactive protein, cystatin C, and white blood cells in ACS were markedly higher than those in healthy volunteers. CA125 was up-regulated in ACS and was a target of miR-203. Injection of miR-203 agomir reduced plaque deposition and vascular thrombosis in the coronary lumen, alleviating myocardial damage. Additionally, miR-203 inhibited myocardial apoptosis and inflammation responses induced by OGD/R and ACS. miR-203 can reduce the inflammatory response by inhibiting CA125 expression, thereby improving ACS symptoms and mitigating ACS-induced myocardial injury.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

miR-203 Alleviates Myocardial Damage Caused by Acute Coronary Syndrome by Inhibiting CA125

  • 期刊论文

  • 发表日期：

    2025年2月28日

查看全文
  • Yanfang Guo,
  • Jinlin Li,
  • Linhao Zhang

摘要

Acute coronary syndrome (ACS) is a significant contributor to cardiovascular mortality. Research has indicated that CA125 levels are linked to cardiovascular disease. This study aimed to explore the role of CA125 in ACS and its underlying mechanism. A retrospective study was conducted involving 34 healthy volunteers and 46 patients diagnosed with ACS. Clinical characteristics and CA125 expression were recorded and detected. Bioinformatics analysis was performed to identify miRNAs that regulate CA125. HL-1 cardiac muscle cells were subjected to oxygen–glucose deprivation/reoxygenation (OGD/R) to investigate the role of CA125 in myocardial injury. An ACS mice model was constructed to further explore the role of CA125 on ACS. The levels of serum creatinine, blood urea nitrogen, uric acid, high-sensitivity C-reactive protein, cystatin C, and white blood cells in ACS were markedly higher than those in healthy volunteers. CA125 was up-regulated in ACS and was a target of miR-203. Injection of miR-203 agomir reduced plaque deposition and vascular thrombosis in the coronary lumen, alleviating myocardial damage. Additionally, miR-203 inhibited myocardial apoptosis and inflammation responses induced by OGD/R and ACS. miR-203 can reduce the inflammatory response by inhibiting CA125 expression, thereby improving ACS symptoms and mitigating ACS-induced myocardial injury.