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Background <p>SRY-box transcription factor 2 (<i>SOX2</i>) is implicated in diverse pathological conditions; however, its contribution to vascular calcification (VC) is not well define. This research explored the influence of <i>SOX2</i> on VC and associated molecular mechanisms utilizing a β-Glycerophosphate (β-GP)-driven calcification model in human aortic vascular smooth muscle cell (HA-VSMC).</p> Results <p>One in vitro VC model was established by exposing HA-VSMCs to β-GP. The experimental design comprised several key groups: an untreated control, a β-GP-induced calcification model group, a group receiving β-GP and <i>SOX2</i>-targeting siRNA (si-<i>SOX2</i>), a group treated with β-GP and 3-Methyladenine (3-MA), an autophagy inhibitor, and a group co-treated with β-GP, si-<i>SOX2</i>, and the Wnt pathway activator BML-284. Relative to controls, the β-GP model group exhibited increased calcification, elevated protein levels of <i>SOX2</i> and osteogenic markers (Runx2, BMP2), enhanced autophagic activity, reduced expression of contractile markers (SM22α, α-SMA), and suppression of Wnt pathway signaling. Transfection with si-<i>SOX2</i> significantly counteracted these β-GP-induced alterations. Conversely, the beneficial impact of si-<i>SOX2</i> on β-GP-induced VC was negated by BML-284-mediated activation of the Wnt pathway.</p> Conclusion <p>The findings indicate that suppressing <i>SOX2</i> alleviates β-GP-induced VC by influencing the activation status of the Wnt pathway.</p>

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Inhibition of SOX2 mitigates vascular calcification mediated by autophagy through Wnt signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月22日

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  • Hui Xiang,
  • Jie Hong,
  • Yingli Zhang,
  • Cong Zeng,
  • Na Wu

摘要

Background

SRY-box transcription factor 2 (SOX2) is implicated in diverse pathological conditions; however, its contribution to vascular calcification (VC) is not well define. This research explored the influence of SOX2 on VC and associated molecular mechanisms utilizing a β-Glycerophosphate (β-GP)-driven calcification model in human aortic vascular smooth muscle cell (HA-VSMC).

Results

One in vitro VC model was established by exposing HA-VSMCs to β-GP. The experimental design comprised several key groups: an untreated control, a β-GP-induced calcification model group, a group receiving β-GP and SOX2-targeting siRNA (si-SOX2), a group treated with β-GP and 3-Methyladenine (3-MA), an autophagy inhibitor, and a group co-treated with β-GP, si-SOX2, and the Wnt pathway activator BML-284. Relative to controls, the β-GP model group exhibited increased calcification, elevated protein levels of SOX2 and osteogenic markers (Runx2, BMP2), enhanced autophagic activity, reduced expression of contractile markers (SM22α, α-SMA), and suppression of Wnt pathway signaling. Transfection with si-SOX2 significantly counteracted these β-GP-induced alterations. Conversely, the beneficial impact of si-SOX2 on β-GP-induced VC was negated by BML-284-mediated activation of the Wnt pathway.

Conclusion

The findings indicate that suppressing SOX2 alleviates β-GP-induced VC by influencing the activation status of the Wnt pathway.