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COVID-19 患者的脂质代谢失调和病理性炎症。

Dysregulation of lipid metabolism and pathological inflammation in patients with COVID-19.

机构信息

CEINGE - Biotecnologie Avanzate s.c.ar.l., Via Gaetano Salvatore, 486, 80145, Naples, Italy.

Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università degli Studi di Napoli "Federico II", 80131, Naples, Italy.

出版信息

Sci Rep. 2021 Feb 3;11(1):2941. doi: 10.1038/s41598-021-82426-7.

DOI:10.1038/s41598-021-82426-7
PMID:33536486
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7859398/
Abstract

In recent months, Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has spread throughout the world. COVID-19 patients show mild, moderate or severe symptoms with the latter ones requiring access to specialized intensive care. SARS-CoV-2 infections, pathogenesis and progression have not been clearly elucidated yet, thus forcing the development of many complementary approaches to identify candidate cellular pathways involved in disease progression. Host lipids play a critical role in the virus life, being the double-membrane vesicles a key factor in coronavirus replication. Moreover, lipid biogenesis pathways affect receptor-mediated virus entry at the endosomal cell surface and modulate virus propagation. In this study, targeted lipidomic analysis coupled with proinflammatory cytokines and alarmins measurement were carried out in serum of COVID-19 patients characterized by different severity degree. Serum IL-26, a cytokine involved in IL-17 pathway, TSLP and adiponectin were measured and correlated to lipid COVID-19 patient profiles. These results could be important for the classification of the COVID-19 disease and the identification of therapeutic targets.

摘要

最近几个月,由严重急性呼吸系统综合症冠状病毒 2(SARS-CoV-2)引起的 2019 年冠状病毒病(COVID-19)在全球范围内传播。COVID-19 患者表现出轻度、中度或重度症状,后者需要进入专门的重症监护病房。SARS-CoV-2 感染、发病机制和进展尚未得到明确阐明,因此需要开发许多补充方法来确定参与疾病进展的候选细胞途径。宿主脂质在病毒生命中起着至关重要的作用,双层膜囊泡是冠状病毒复制的关键因素。此外,脂质生物发生途径影响受体介导的病毒进入内体细胞表面,并调节病毒增殖。在这项研究中,对不同严重程度的 COVID-19 患者的血清进行了靶向脂质组学分析,并结合促炎细胞因子和警报素的测量。测量了细胞因子 IL-26(参与 IL-17 途径)、TSLP 和脂联素,并将其与 COVID-19 患者的脂质谱相关联。这些结果对于 COVID-19 疾病的分类和治疗靶点的确定可能很重要。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb89/7859398/0f95fafb42fe/41598_2021_82426_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb89/7859398/99f252696c55/41598_2021_82426_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb89/7859398/e9106e9c3886/41598_2021_82426_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb89/7859398/0f95fafb42fe/41598_2021_82426_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb89/7859398/99f252696c55/41598_2021_82426_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb89/7859398/e9106e9c3886/41598_2021_82426_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb89/7859398/0f95fafb42fe/41598_2021_82426_Fig3_HTML.jpg

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2
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Int J Mol Sci. 2020 Jul 15;21(14):4998. doi: 10.3390/ijms21144998.
3
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Adv Sci (Weinh). 2025 Sep;12(33):e15181. doi: 10.1002/advs.202415181. Epub 2025 Jun 17.
6
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7
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Front Cell Dev Biol. 2025 Mar 5;13:1476329. doi: 10.3389/fcell.2025.1476329. eCollection 2025.
8
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8
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