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Lkb1 ダウンレギュレーション PVAT リフォームと大動脈拡張または動脈瘤の関連

Zhaohua Cai¹, Min Liang¹, Yangjing Jiang¹

¹Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Circulation research

|August 28, 2025

まとめ

周血管脂肪組織 (PVAT) の肝臓キナーゼB1 (Lkb1) 欠乏は,大動脈の膨張と動脈瘤を引き起こす. PVATにおけるレニン- 血管新生システムの回復は,これらの血管疾患を予防します.

科学分野:

心血管生物学
血管の生理学
脂肪組織生物学

背景:

血管周脂肪組織 (PVAT) は血管の恒常性と疾患を調節する.
肝臓キナーゼB1 (Lkb1) は癌と心血管疾患に関連しています.

研究の目的:

PVATにおける Lkb1の役割とその血管機能への影響を調査する.
Lkb1が血管の健康に影響を与えるメカニズムを決定する.

主な方法:

タモキシフェン誘導のLkb1条件付きノックアウトマウスモデル (Lkb1flox/flox;Pdgfrα-CreERT2,Lkb1flox/flox;Pdgfrβ-CreERT2,Lkb1flox/flox;Myh11-CreERT2) を生成した.
アンジオテンシンII誘発性大動脈瘤におけるLkb1発現とそのダウンレギュレーションの評価
様々なPVAT細胞のLkb1欠乏が血管機能に与える影響を分析した.

主要な成果:

Lkb1は,大動脈動脈形成中にPVATでダウンレギュレーションされます.
Pdgfrα+,Myh11+,またはPdgfrβ+細胞のLkb1欠乏はPVAT機能障害を引き起こし,大動脈の拡張と動脈瘤を引き起こす.
Lkb1の遺伝的消去はPVATレニン- 血管新生系を活性化し,血管滑らかな筋肉細胞 (VSMC) のフェノタイプスイッチングを促進します.
アリスキレンまたはヴァルサルタン治療は,Lkb1欠乏したマウスのVSMCの切り替えと大動脈の拡張を救った.

結論:

PVATのLkb1欠乏はVSMCのフェノタイプスイッチを誘導し,大動脈の拡張と動脈瘤を引き起こす.
Lkb1は,血管ホメオスタシスを維持するために,PVATにおけるレニン-アニオテンシンシステムを調節する.

キーワード:

脂肪組織大動脈動脈瘤膨張ホメオスタシスレニン

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