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[Not Available].[无可用内容]。
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本文引用的文献

1
sST2 as a value-added biomarker in heart failure.sST2 作为心力衰竭的增值标志物。
Clin Chim Acta. 2020 Feb;501:120-130. doi: 10.1016/j.cca.2019.10.029. Epub 2019 Oct 31.
2
ST2 and the ST2/IL-33 signalling pathway-biochemistry and pathophysiology in animal models and humans.ST2 及其 ST2/IL-33 信号通路:动物模型和人类的生物化学和病理生理学。
Clin Chim Acta. 2019 Aug;495:493-500. doi: 10.1016/j.cca.2019.05.023. Epub 2019 May 25.
3
Cardiac Biomarkers in the Emergency Department: The Role of Soluble ST2 (sST2) in Acute Heart Failure and Acute Coronary Syndrome-There is Meat on the Bone.急诊科中的心脏生物标志物:可溶性ST2(sST2)在急性心力衰竭和急性冠状动脉综合征中的作用——确有实质内容。
J Clin Med. 2019 Feb 22;8(2):270. doi: 10.3390/jcm8020270.
4
Elevated Sera sST2 Is Associated With Heart Failure in Men ≤50 Years Old With Myocarditis.血清 sST2 水平升高与<50 岁伴心肌炎的心力衰竭男性患者相关。
J Am Heart Assoc. 2019 Jan 22;8(2):e008968. doi: 10.1161/JAHA.118.008968.
5
Clinical pharmacogenomics of carvedilol: the stereo-selective metabolism angle.卡维地洛的临床药物基因组学:立体选择性代谢视角
Pharmacogenomics. 2018 Sep 1;19(14):1089-1093. doi: 10.2217/pgs-2018-0115. Epub 2018 Aug 8.
6
Impact of CYP2D6 Genetic Variation on the Response of the Cardiovascular Patient to Carvedilol and Metoprolol.CYP2D6基因变异对心血管疾病患者对卡维地洛和美托洛尔反应的影响。
Curr Drug Metab. 2015;17(1):30-6. doi: 10.2174/1389200217666151105125425.
7
Head-to-head comparison of serial soluble ST2, growth differentiation factor-15, and highly-sensitive troponin T measurements in patients with chronic heart failure.比较慢性心力衰竭患者连续可溶性 ST2、生长分化因子-15 和高敏肌钙蛋白 T 的头对头研究
JACC Heart Fail. 2014 Feb;2(1):65-72. doi: 10.1016/j.jchf.2013.10.005. Epub 2014 Jan 25.
8
Chronic heart failure: current evidence, challenges to therapy, and future directions.慢性心力衰竭:当前的证据、治疗面临的挑战和未来方向。
Am J Cardiovasc Drugs. 2011 Jun 1;11(3):153-71. doi: 10.2165/11592090-000000000-00000.
9
Interleukin-33 biology with potential insights into human diseases.白细胞介素-33 生物学及其对人类疾病的潜在影响。
Nat Rev Rheumatol. 2011 Jun;7(6):321-9. doi: 10.1038/nrrheum.2011.53. Epub 2011 Apr 26.
10
The IL-33/ST2 pathway--A new therapeutic target in cardiovascular disease.IL-33/ST2 通路——心血管疾病的新治疗靶点。
Pharmacol Ther. 2011 Aug;131(2):179-86. doi: 10.1016/j.pharmthera.2011.02.005. Epub 2011 Feb 26.

白细胞介素-33和可溶性ST2的生物标志物及其与心力衰竭中卡维地洛治疗的无关联

Biomarkers of IL-33 and sST2 and Lack of Association with Carvedilol Therapy in Heart Failure.

作者信息

Firouzabadi Negar, Dashti Maryam, Dehshahri Ali, Bahramali Ehsan

机构信息

Department of Pharmacology and Toxicology, School of Pharmacy, Shiraz University of Medical Sciences, Shiraz, Iran.

Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

出版信息

Clin Pharmacol. 2020 Jun 12;12:53-58. doi: 10.2147/CPAA.S256290. eCollection 2020.

DOI:10.2147/CPAA.S256290
PMID:32607003
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7305854/
Abstract

OBJECTIVE

The IL-33/ST2 pathway plays a fundamental role in the cardiovascular system and can be considered as a new therapeutic strategy for the treatment or prevention of cardiovascular diseases. ST2, as an interleukin (IL)-1 receptor family member, has transmembrane (ST2L) and soluble (sST2) isoforms. sST2 neutralizes IL-33 and thereby inhibits the cardioprotective role of IL-33/ST2L signaling pathway. Increase in sST2 level is associated with weak cardiac output and can be a predictor of mortality in heart failure (HF). Thereby, we hypothesized that there may be a relationship between the cardioprotective effects of carvedilol and sST2 and IL-3 in HF patients.

METHODS

sST2 and IL-33 were measured in serum of 66 individuals; 22 healthy volunteers and 44 suffering from HF; among whom 25 patients received carvedilol and the other 19 patients did not receive any β-blockers.

RESULTS

Lack of association between serum levels of IL-33 and sST2 was observed between HF patients and healthy individuals (2.4466 ± 0.69 vs 2.6748 ± 0.33 and 3416.6 ± 1089.1 vs 2971.6 ± 792.5, respectively). Our results indicated no significant difference between sST2 and IL-33 levels in HF patients who did not receive beta-blockers and patients receiving carvedilol (P=0.59 and P=0.97).

CONCLUSION

Our results showed a lack of association between serum levels of IL-33 and sST2 and HF. Moreover, the results do not confirm the cardioprotective mechanism of carvedilol by means of IL-33/sST2 pathway.

摘要

目的

白细胞介素(IL)-33/ST2通路在心血管系统中起重要作用,可被视为治疗或预防心血管疾病的一种新的治疗策略。ST2作为白细胞介素-1受体家族成员,有跨膜(ST2L)和可溶性(sST2)两种亚型。sST2可中和IL-33,从而抑制IL-33/ST2L信号通路的心脏保护作用。sST2水平升高与心输出量降低有关,可作为心力衰竭(HF)患者死亡率的预测指标。因此,我们推测卡维地洛的心脏保护作用与HF患者的sST2和IL-3之间可能存在关联。

方法

检测了66例个体血清中的sST2和IL-33;其中22例为健康志愿者,44例为HF患者;44例HF患者中,25例接受了卡维地洛治疗,另外19例未接受任何β受体阻滞剂治疗。

结果

HF患者与健康个体血清IL-33和sST2水平之间无相关性(分别为2.4466±0.69 vs 2.6748±0.33和3416.6±1089.1 vs 2971.6±792.5)。我们的结果表明,未接受β受体阻滞剂治疗的HF患者与接受卡维地洛治疗的患者之间,sST2和IL-33水平无显著差异(P=0.59和P=0.97)。

结论

我们的结果表明,血清IL-33和sST2水平与HF之间无相关性。此外,结果未证实卡维地洛通过IL-33/sST2通路发挥心脏保护作用的机制。