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抑制MALAT1通过Keap1/HO-1通路促进ROS积累,以增强二次性副甲状腺功能障碍症的光动力疗法

Ying Wen¹, Yitong Li^1,2, Danhua Zhang¹

¹Department of General Surgery, The Second Xiangya Hospital, Central South University, Clinical Research Center for Breast Disease in Hunan Province, Changsha, Hunan, 410011, China.

Non-coding RNA research

|February 3, 2025

概括

对于二次性甲状腺功能障碍症 (SHPT) 的光动力疗法 (PDT) 通过抑制长非编码RNA的MALAT1来增强. 这种抑制促进了活性氧物种 (ROS) 和亡,提高了PDT在SHPT治疗中的疗效.

科学领域:

生物化学生物化学
分子生物学分子生物学
在瘤学瘤学.

背景情况:

二次性偏甲状腺症 (SHPT) 影响超过80%的晚期慢性病 (CKD) 患者.
光动力疗法 (PDT) 显示出对SHPT治疗的前景.
在SHPT中PDT的分子机制,特别是涉及长非编码RNA (lncRNAs),尚未完全理解.

研究的目的:

为了研究PDT在SHPT中的分子机制.
探索长非编码RNAMALAT1在PDT诱导的亡和SHPT中反应性氧物种 (ROS) 生成中的作用.
评估MALAT1作为一种潜在的治疗点,以提高SHPT中的PDT疗效.

主要方法:

研究PDT对SHPT细胞的影响,重点关注ROS积累和亡.
使用定量方法分析了PDT后的MALAT1和HO-1表达.
利用RNA pulldown,西部抹杀和高通量测序来确认MALAT1,Keap1和HO-1之间的相互作用.
评估了MALAT1抑制和HO-1过度表达对ROS水平和亡的影响.
在SHPT大鼠模型中评估了PDT和MALAT1抑制剂对副甲状腺激素 (PTH) 分泌的联合作用.

主要成果:

在SHPT中通过ROS积累引起PDT诱导的亡.
在PDT上调调节了SHPT中的MALAT1和HO-1表达.
抑制MALAT1增加了ROS并促进了亡,而HO-1过度表达逆转了这些影响.
MALAT1直接与Keap1结合,调节HO-1表达和随后的ROS水平.
抑制MALAT1增强了PDT在减少SHPT大鼠PTH分泌中的有效性.

结论:

MALAT1通过与Keap1结合激活HO-1,减少ROS和抑制亡,从而在SHPT中赋予PDT耐药性.
抑制MALAT1显著提高了SHPT的PDT疗效.
马拉特1代表了一种有前途的治疗标,用于改善SHPT的PDT结果.

关键词:

长链非编码RNA是什么光动力学疗法是一种光动力学疗法.有反应性氧物种的反应性氧物种.二次性副甲状腺功能障碍症的发生.

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