综合生物信息学和验证显示,PTGS2及其相关分子可缓解TNF-α诱导的内皮衰老
Hongjie Xu1, He Wang1, Xiaoping Ning1
1Department of Cardiovascular Surgery, Changhai Hospital, The Naval Medical University, 168 Changhai Road, Shanghai, 200433, China.
In vitro cellular & developmental biology. Animal
|June 10, 2024
概括
细胞衰老和铁灭相互作用. 这项研究确定了TNF-α诱导的内皮衰老中的铁灭标志物,发现了PTGS2并验证了氨基酸作为衰老HUVECs的潜在治疗药物.
科学领域:
- 生物医学研究的研究.
- 分子生物学分子生物学
- 细胞衰老 细胞衰老
背景情况:
- 细胞衰老和铁亡越来越多地被认为是相互作用的生物过程.
- 瘤亡因子-α (TNF-α) 可以诱导内皮衰老,这种状态与各种病理有关.
- 了解连接这些过程的分子机制对于治疗开发至关重要.
研究的目的:
- 在TNF-α诱导的人类静脉内皮细胞 (HUVEC) 衰老中研究与铁灭相关的分子标记物.
- 确定潜在的治疗点和药物,通过铁死来缓解内皮老化.
主要方法:
- 在微阵列数据 (GSE195517) 上进行权重基因协同表达网络分析 (WGCNA),以识别差异表达的铁相关基因 (DEFRGs).
- 基因本体学 (GO) 和基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因基因.
- 蛋白与蛋白相互作用 (PPI) 网络构建以识别中心基因,通过RT-qPCR验证.
- 药物基因网络分析用于预测潜在药物.
主要成果:
- 在TNF-α诱导的HUVEC衰老中发现了七种DEFRG.
- 四个升调的枢纽基因 (PTGS2,TNFAIP3,CXCL2,IL6) 得到了验证.
- PTGS2局部存在于血膜中.
- 氨基酸 (ASA) 被确定为潜在的铁灭抑制剂,向PTGS2;5-ASA和4-ASA在缓解衰老方面表现出有效性.
结论:
- PTGS2在TNF-α诱导的HUVEC衰老中发挥着重要作用.
- 氨基酸 (ASA) 显示出作为治疗剂的潜力,通过向铁亡来缓解内皮衰老.
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