• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

肺动脉高压的细胞因子谱:氧化还原平衡和性别作用。

Cytokine profiling in pulmonary arterial hypertension: the role of redox homeostasis and sex.

机构信息

Department of Medicine, University of Arizona College of Medicine, Tucson, Arizona.

Department of Medicine, University of California San Diego, La Jolla, California.

出版信息

Transl Res. 2022 Sep;247:1-18. doi: 10.1016/j.trsl.2022.03.013. Epub 2022 Apr 9.

DOI:10.1016/j.trsl.2022.03.013
PMID:35405322
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10062382/
Abstract

Pulmonary arterial hypertension (PAH) is a fatal disease with a well-established sexual dimorphism. Activated inflammatory response and altered redox homeostasis, both known to manifest in a sex-specific manner, are implicated in the pathogenic mechanisms involved in PAH development. This study aimed to evaluate the impact of sex and plasma redox status on circulating cytokine profiles. Plasma oxidation-reduction potential (ORP), as a substitute measure of redox status, was analyzed in male and female Group 1 PAH and healthy subjects. The profiles of 27 circulating cytokines were compared in 2 PAH groups exhibiting the highest and lowest quartile for plasma ORP, correlated with clinical parameters, and used to predict patient survival. The analysis of the PAH groups with the highest and lowest ORP revealed a correlation between elevated cytokine levels and increased oxidative stress in females. In contrast, in males, cytokine expressions were increased in the lower oxidative environment (except for IL-1b). Correlations of the increased cytokine expressions with PAH severity were highly sex-dependent and corresponded to the increase in PAH severity in males and less severe PAH in females. Machine learning algorithms trained on the combined cytokine and redox profiles allowed the prediction of PAH mortality with 80% accuracy. We conclude that the profile of circulating cytokines in PAH patients is redox- and sex-dependent, suggesting the vital need to stratify the patient cohort subjected to anti-inflammatory therapies. Combined cytokine and/or redox profiling showed promising value for predicting the patients' survival.

摘要

肺动脉高压(PAH)是一种致命疾病,具有明确的性别二态性。已证实,以性别特异性方式表现的激活炎症反应和改变氧化还原稳态与 PAH 发展相关的致病机制有关。本研究旨在评估性别和血浆氧化还原状态对循环细胞因子谱的影响。氧化还原电位(ORP)作为氧化还原状态的替代测量指标,在 1 组男性和女性 PAH 以及健康受试者中进行了分析。比较了 27 种循环细胞因子在 2 组 PAH 患者中的分布,这 2 组 PAH 患者的血浆 ORP 最高和最低四分位数,与临床参数相关,并用于预测患者的生存。对 ORP 最高和最低的 PAH 组进行分析表明,女性的细胞因子水平升高与氧化应激增加之间存在相关性。相比之下,在男性中,细胞因子表达在较低的氧化环境中增加(除了 IL-1b)。细胞因子表达增加与 PAH 严重程度的相关性具有高度性别依赖性,与男性 PAH 严重程度增加和女性 PAH 严重程度降低相对应。基于组合细胞因子和氧化还原谱的机器学习算法可准确预测 80%的 PAH 死亡率。我们得出结论,PAH 患者的循环细胞因子谱是氧化还原和性别依赖性的,这表明迫切需要对接受抗炎治疗的患者队列进行分层。联合细胞因子和/或氧化还原谱显示出预测患者生存的有希望的价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f4/10062382/525c85ba52b0/nihms-1882602-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f4/10062382/3f3b68779074/nihms-1882602-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f4/10062382/0c432d06b9a3/nihms-1882602-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f4/10062382/3496d185ec8b/nihms-1882602-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f4/10062382/603fa3c9a9d4/nihms-1882602-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f4/10062382/525c85ba52b0/nihms-1882602-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f4/10062382/3f3b68779074/nihms-1882602-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f4/10062382/0c432d06b9a3/nihms-1882602-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f4/10062382/3496d185ec8b/nihms-1882602-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f4/10062382/603fa3c9a9d4/nihms-1882602-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/07f4/10062382/525c85ba52b0/nihms-1882602-f0005.jpg

相似文献

1
Cytokine profiling in pulmonary arterial hypertension: the role of redox homeostasis and sex.肺动脉高压的细胞因子谱:氧化还原平衡和性别作用。
Transl Res. 2022 Sep;247:1-18. doi: 10.1016/j.trsl.2022.03.013. Epub 2022 Apr 9.
2
Gender Difference in Damage-Mediated Signaling Contributes to Pulmonary Arterial Hypertension.性别差异在损伤介导的信号转导中起作用,导致肺动脉高压。
Antioxid Redox Signal. 2019 Nov 1;31(13):917-932. doi: 10.1089/ars.2018.7664. Epub 2019 Mar 20.
3
Plasma markers in pulmonary hypertension subgroups correlate with patient survival.肺高血压亚组中的血浆标志物与患者生存率相关。
Respir Res. 2021 May 4;22(1):137. doi: 10.1186/s12931-021-01716-w.
4
Cytokine signatures differentiate systemic sclerosis patients at high versus low risk for pulmonary arterial hypertension.细胞因子特征可区分系统性硬化症患者发生肺动脉高压的高风险与低风险。
Arthritis Res Ther. 2022 Feb 9;24(1):39. doi: 10.1186/s13075-022-02734-9.
5
Severe Pulmonary Arterial Hypertension Is Characterized by Increased Neutrophil Elastase and Relative Elafin Deficiency.严重肺动脉高压的特征是中性粒细胞弹性蛋白酶增加和相对 Elafin 缺乏。
Chest. 2021 Oct;160(4):1442-1458. doi: 10.1016/j.chest.2021.06.028. Epub 2021 Jun 26.
6
Necrosis-Released HMGB1 (High Mobility Group Box 1) in the Progressive Pulmonary Arterial Hypertension Associated With Male Sex.在与男性相关的进行性肺动脉高压中,坏死释放的高迁移率族蛋白 B1(HMGB1)。
Hypertension. 2020 Dec;76(6):1787-1799. doi: 10.1161/HYPERTENSIONAHA.120.16118. Epub 2020 Oct 5.
7
Pulmonary arterial hypertension induces the release of circulating extracellular vesicles with oxidative content and alters redox and mitochondrial homeostasis in the brains of rats.肺动脉高压诱导循环细胞外囊泡释放具有氧化含量,并改变大鼠大脑中的氧化还原和线粒体动态平衡。
Hypertens Res. 2021 Aug;44(8):918-931. doi: 10.1038/s41440-021-00660-y. Epub 2021 Apr 19.
8
Discovery of Distinct Immune Phenotypes Using Machine Learning in Pulmonary Arterial Hypertension.利用机器学习在肺动脉高压中发现不同的免疫表型。
Circ Res. 2019 Mar 15;124(6):904-919. doi: 10.1161/CIRCRESAHA.118.313911.
9
Role of Gender in Regulation of Redox Homeostasis in Pulmonary Arterial Hypertension.性别在肺动脉高压氧化还原稳态调节中的作用
Antioxidants (Basel). 2019 May 16;8(5):135. doi: 10.3390/antiox8050135.
10
Cytokines, Chemokines, and Inflammation in Pulmonary Arterial Hypertension.细胞因子、趋化因子与肺动脉高压中的炎症反应。
Adv Exp Med Biol. 2021;1303:275-303. doi: 10.1007/978-3-030-63046-1_15.

引用本文的文献

1
Microbiota Transplant Therapy Is Safe and Feasible in Pulmonary Arterial Hypertension.微生物群移植疗法在肺动脉高压中是安全可行的。
JACC Basic Transl Sci. 2025 Aug 12;10(9):101347. doi: 10.1016/j.jacbts.2025.101347.
2
Characteristic disease defects in circulating endothelial cells isolated from patients with pulmonary arterial hypertension.从肺动脉高压患者循环内皮细胞中分离出的特征性疾病缺陷。
PLoS One. 2024 Oct 28;19(10):e0312535. doi: 10.1371/journal.pone.0312535. eCollection 2024.
3
Circulating free heme induces cytokine storm and pulmonary hypertension through the MKK3/p38 axis.

本文引用的文献

1
Neutrophil-Lymphocyte Ratio as an Independent Predictor of Survival in Pulmonary Arterial Hypertension: An Exploratory Study.中性粒细胞与淋巴细胞比值作为肺动脉高压患者生存的独立预测指标:一项探索性研究
CJC Open. 2021 Nov 29;4(4):357-363. doi: 10.1016/j.cjco.2021.11.010. eCollection 2022 Apr.
2
Necrosis-Released HMGB1 (High Mobility Group Box 1) in the Progressive Pulmonary Arterial Hypertension Associated With Male Sex.在与男性相关的进行性肺动脉高压中,坏死释放的高迁移率族蛋白 B1(HMGB1)。
Hypertension. 2020 Dec;76(6):1787-1799. doi: 10.1161/HYPERTENSIONAHA.120.16118. Epub 2020 Oct 5.
3
Greater high-mobility group box 1 in male compared with female spontaneously hypertensive rats worsens renal ischemia-reperfusion injury.
循环游离血红素通过 MKK3/p38 轴诱导细胞因子风暴和肺动脉高压。
Am J Physiol Lung Cell Mol Physiol. 2024 Oct 1;327(4):L574-L586. doi: 10.1152/ajplung.00422.2022. Epub 2024 Aug 28.
4
Deciphering the Complexities of Pulmonary Hypertension: The Emergent Role of Single-Cell Omics.解读肺动脉高压的复杂性:单细胞组学的新兴作用
Am J Respir Cell Mol Biol. 2024 Aug 14;72(1):32-40. doi: 10.1165/rcmb.2024-0145PS.
5
EnFUSiasm for Healing: Ultrasound Neuromodulation in PAH.治愈的热情:超声神经调节在肺动脉高压中的应用
Circ Res. 2024 Jun 21;135(1):57-59. doi: 10.1161/CIRCRESAHA.124.324791. Epub 2024 Jun 20.
6
Endothelial periostin regulates vascular remodeling by promoting endothelial dysfunction in pulmonary arterial hypertension.内皮细胞骨膜蛋白通过促进肺动脉高压中的内皮功能障碍来调节血管重塑。
Anim Cells Syst (Seoul). 2024 Jan 3;28(1):1-14. doi: 10.1080/19768354.2023.2300437. eCollection 2024.
7
Hypoxia-induced pulmonary hypertension upregulates eNOS and TGF-β contributing to sex-linked differences in mutant mice.缺氧诱导的肺动脉高压上调内皮型一氧化氮合酶(eNOS)和转化生长因子-β(TGF-β),这导致了突变小鼠的性别差异。
Pulm Circ. 2022 Oct 1;12(4):e12163. doi: 10.1002/pul2.12163. eCollection 2022 Oct.
雄性自发性高血压大鼠中高迁移率族蛋白 B1 的增加程度高于雌性大鼠,会加重肾缺血再灌注损伤。
Clin Sci (Lond). 2020 Jul 17;134(13):1751-1762. doi: 10.1042/CS20200575.
4
Sex-specific stress response and HMGB1 release in pulmonary endothelial cells.肺血管内皮细胞中性别特异性应激反应和高迁移率族蛋白 B1 的释放。
PLoS One. 2020 Apr 9;15(4):e0231267. doi: 10.1371/journal.pone.0231267. eCollection 2020.
5
Early progression of pulmonary hypertension in the monocrotaline model in males is associated with increased lung permeability.雄性野百合碱模型中肺动脉高压的早期进展与肺通透性增加有关。
Biol Sex Differ. 2020 Mar 18;11(1):11. doi: 10.1186/s13293-020-00289-5.
6
Cellular sources of interleukin-6 and associations with clinical phenotypes and outcomes in pulmonary arterial hypertension.细胞来源的白细胞介素-6 及其与肺动脉高压临床表型和结局的相关性。
Eur Respir J. 2020 Apr 16;55(4). doi: 10.1183/13993003.01761-2019. Print 2020 Apr.
7
Pulmonary Capillary Hemangioma-like Pulmonary Artery Hypertension Associated With Interferon-Alpha Therapy.与α-干扰素治疗相关的肺毛细血管瘤样肺动脉高压
Am J Ther. 2020 Sep/Oct;27(5):e511-e514. doi: 10.1097/MJT.0000000000001141.
8
Sex, Gender, and Sex Hormones in Pulmonary Hypertension and Right Ventricular Failure.肺动脉高压与右心衰竭中的性别、性别差异和性激素。
Compr Physiol. 2019 Dec 18;10(1):125-170. doi: 10.1002/cphy.c190011.
9
Necrosis Contributes to the Development of Hypertension in Male, but Not Female, Spontaneously Hypertensive Rats.坏死导致雄性自发性高血压大鼠高血压的发展,但对雌性大鼠则没有影响。
Hypertension. 2019 Dec;74(6):1524-1531. doi: 10.1161/HYPERTENSIONAHA.119.13477. Epub 2019 Oct 28.
10
The Diversification of Cell Death and Immunity: Memento Mori.细胞死亡与免疫的多样化:记住死亡。
Mol Cell. 2019 Oct 17;76(2):232-242. doi: 10.1016/j.molcel.2019.09.006. Epub 2019 Oct 2.