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Multi-biobank summary data Mendelian randomisation does not support a causal effect of IL-6 signalling on risk of pulmonary arterial hypertension
European Respiratory Journal ( IF 24.3 ) Pub Date : 2024-04-04
Woolf, B., Perry, J. A., Hong, C. C., Wilkins, M. R., Toshner, M., Gill, D., Burgess, S., Rhodes, C. J.

Extract

Interleukin (IL)-6 has been linked with the pathobiology of pulmonary arterial hypertension (PAH). IL-6 plasma levels are elevated in PAH patients and closely linked to survival [1]. Both increased IL-6 activity and gene knockout influence the development of, and resistance to, pulmonary hypertension in animal models [2–4]. IL-6 can repress expression of BMPR2, a gene key in PAH risk [5].



中文翻译:

多生物库汇总数据孟德尔随机化不支持 IL-6 信号传导对肺动脉高压风险的因果影响

提炼

白介素 (IL)-6 与肺动脉高压 (PAH) 的病理学有关。 PAH 患者血浆 IL-6 水平升高,与生存密切相关[1]。 IL-6 活性增加和基因敲除都会影响动物模型中肺动脉高压的发展和抵抗力 [2-4]。 IL-6 可以抑制BMPR2 的表达, BMPR2 是 PAH 风险的关键基因 [5]。

更新日期:2024-04-04
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