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Objective <p>To explore the protective mechanism of HIF-1α on coronary atherosclerosis (CA) through the IL-6/JAK1/STAT3 pathway.</p> Methods <p>Forty rats were randomly divided into control group, model group, OE HIF-1α group, and shRNA HIF-1α group. The morphology of coronary arteries, ROS fluorescence intensity, measure myocardial enzyme spectrum, and serum biochemical indicators were observed. The expression of HIF-1α, IL-6/JAK1/STAT3 proteins in myocardial tissue was detected by Western blot.</p> Results <p>Compared to controls, CA model rats exhibited significantly increased HIF-1α expression (1.7-fold in serum, 2.5-fold in myocardium), elevated ROS levels (2.1-fold), activated IL-6/JAK1/STAT3 pathway (3.2-fold), and coronary artery dilation (79% wider), alongside worsened myocardial enzymes and serum lipids (all <i>P</i> &lt; 0.05); HIF-1α knockdown reversed these changes, reducing HIF-1α by 35%, ROS by 40%, pathway activity by 50%, and coronary diameter by 25%, while HIF-1α overexpression exacerbated all parameters with 2.8-fold higher HIF-1α, 90% increased ROS, and 3.5-fold pathway activation (all <i>P</i> &lt; 0.01).</p> Conclusion <p>HIF-1α knockdown attenuates CA by suppressing IL-6/JAK1/STAT3, reducing oxidative stress and vascular remodeling, while overexpression worsens outcomes. These findings highlight HIF-1α as a potential therapeutic target for CA, suggesting that its inhibition could mitigate myocardial injury in ischemic heart disease.</p>

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The role of HIF-1α in rat coronary atherosclerosis through the IL-6/JAK1/STAT3 pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月5日

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  • Hui Huang,
  • Xiuze Zhang,
  • Ping Liu,
  • Jingyu Zhang

摘要

Objective

To explore the protective mechanism of HIF-1α on coronary atherosclerosis (CA) through the IL-6/JAK1/STAT3 pathway.

Methods

Forty rats were randomly divided into control group, model group, OE HIF-1α group, and shRNA HIF-1α group. The morphology of coronary arteries, ROS fluorescence intensity, measure myocardial enzyme spectrum, and serum biochemical indicators were observed. The expression of HIF-1α, IL-6/JAK1/STAT3 proteins in myocardial tissue was detected by Western blot.

Results

Compared to controls, CA model rats exhibited significantly increased HIF-1α expression (1.7-fold in serum, 2.5-fold in myocardium), elevated ROS levels (2.1-fold), activated IL-6/JAK1/STAT3 pathway (3.2-fold), and coronary artery dilation (79% wider), alongside worsened myocardial enzymes and serum lipids (all P < 0.05); HIF-1α knockdown reversed these changes, reducing HIF-1α by 35%, ROS by 40%, pathway activity by 50%, and coronary diameter by 25%, while HIF-1α overexpression exacerbated all parameters with 2.8-fold higher HIF-1α, 90% increased ROS, and 3.5-fold pathway activation (all P < 0.01).

Conclusion

HIF-1α knockdown attenuates CA by suppressing IL-6/JAK1/STAT3, reducing oxidative stress and vascular remodeling, while overexpression worsens outcomes. These findings highlight HIF-1α as a potential therapeutic target for CA, suggesting that its inhibition could mitigate myocardial injury in ischemic heart disease.