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炎症衰老时钟敲响!——IL-11 登场!

The inflammaging clock strikes IL-11!

机构信息

Division of Cellular & Molecular Biology, Diabetes Research Group, Toronto General Hospital Research Institute (TGHRI), University Health Network, Toronto, ON M5G 1L7, Canada.

Division of Cellular & Molecular Biology, Diabetes Research Group, Toronto General Hospital Research Institute (TGHRI), University Health Network, Toronto, ON M5G 1L7, Canada; Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON M5S 1A8, Canada.

出版信息

Immunity. 2024 Sep 10;57(9):2010-2012. doi: 10.1016/j.immuni.2024.08.010.

DOI:10.1016/j.immuni.2024.08.010
PMID:39260354
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11449161/
Abstract

Chronic inflammation is considered a hallmark of aging. In a recent issue of Nature, Widjaja et al. examined genetic and pharmacologic inhibition of interleukin (IL)-11 on aging pathology and found that inhibiting IL-11 signaling increases lifespan and healthspan in mice.

摘要

慢性炎症被认为是衰老的一个标志。在最近的一期《自然》杂志上,Widjaja 等人研究了白细胞介素 (IL)-11 的遗传和药理学抑制对衰老病理的影响,发现抑制 IL-11 信号通路可以增加小鼠的寿命和健康寿命。

相似文献

1
The inflammaging clock strikes IL-11!炎症衰老时钟敲响!——IL-11 登场!
Immunity. 2024 Sep 10;57(9):2010-2012. doi: 10.1016/j.immuni.2024.08.010.
2
Pro-inflammatory cytokine 11 plays a pivotal role in inflammaging-associated pathologies.促炎细胞因子 11 在与炎症相关的病理中起着关键作用。
Aging Cell. 2024 Nov;23(11):e14360. doi: 10.1111/acel.14360. Epub 2024 Oct 3.
3
Defying "IL-11ness" by inhibiting inflammation: Strategy for health and longevity.通过抑制炎症来对抗“IL-11 疾病”:健康长寿的策略。
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Arch Immunol Ther Exp (Warsz). 2016 Apr;64(2):111-26. doi: 10.1007/s00005-015-0377-3. Epub 2015 Dec 12.
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Downregulation of the NF-κB protein p65 is a shared phenotype among most anti-aging interventions.核因子κB蛋白p65的下调是大多数抗衰老干预措施共有的表型。
Geroscience. 2024 Dec 12. doi: 10.1007/s11357-024-01466-9.
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本文引用的文献

1
Inhibition of IL-11 signalling extends mammalian healthspan and lifespan.抑制 IL-11 信号转导可延长哺乳动物的健康寿命和寿命。
Nature. 2024 Aug;632(8023):157-165. doi: 10.1038/s41586-024-07701-9. Epub 2024 Jul 17.
2
IL-11 induces NLRP3 inflammasome activation in monocytes and inflammatory cell migration to the central nervous system.白细胞介素-11 诱导单核细胞中 NLRP3 炎性小体的激活和炎症细胞向中枢神经系统的迁移。
Proc Natl Acad Sci U S A. 2023 Jun 27;120(26):e2221007120. doi: 10.1073/pnas.2221007120. Epub 2023 Jun 20.
3
Chronic inflammation and the hallmarks of aging.
慢性炎症与衰老的特征。
Mol Metab. 2023 Aug;74:101755. doi: 10.1016/j.molmet.2023.101755. Epub 2023 Jun 15.
4
IL11 Stimulates IL33 Expression and Proinflammatory Fibroblast Activation across Tissues.IL11 可刺激多种组织中的 IL33 表达和促炎成纤维细胞活化。
Int J Mol Sci. 2022 Aug 10;23(16):8900. doi: 10.3390/ijms23168900.
5
Tuning immunity through tissue mechanotransduction.通过组织机械转导来调节免疫。
Nat Rev Immunol. 2023 Mar;23(3):174-188. doi: 10.1038/s41577-022-00761-w. Epub 2022 Aug 16.
6
IL-33 causes thermogenic failure in aging by expanding dysfunctional adipose ILC2.IL-33 通过扩张功能失调的脂肪组织 ILC2 导致衰老时的产热功能障碍。
Cell Metab. 2021 Nov 2;33(11):2277-2287.e5. doi: 10.1016/j.cmet.2021.08.004. Epub 2021 Sep 1.
7
Interleukin-11-expressing fibroblasts have a unique gene signature correlated with poor prognosis of colorectal cancer.表达白细胞介素-11 的成纤维细胞具有独特的基因特征,与结直肠癌的不良预后相关。
Nat Commun. 2021 Apr 16;12(1):2281. doi: 10.1038/s41467-021-22450-3.
8
Hiding in Plain Sight: Interleukin-11 Emerges as a Master Regulator of Fibrosis, Tissue Integrity, and Stromal Inflammation.掩人耳目:白细胞介素-11 成为纤维化、组织完整性和基质炎症的主要调节因子。
Annu Rev Med. 2020 Jan 27;71:263-276. doi: 10.1146/annurev-med-041818-011649.
9
IL-11 is a crucial determinant of cardiovascular fibrosis.白细胞介素-11是心血管纤维化的关键决定因素。
Nature. 2017 Dec 7;552(7683):110-115. doi: 10.1038/nature24676. Epub 2017 Nov 13.
10
IL-11 Induces Th17 Cell Responses in Patients with Early Relapsing-Remitting Multiple Sclerosis.白细胞介素-11在早期复发缓解型多发性硬化症患者中诱导Th17细胞反应。
J Immunol. 2015 Jun 1;194(11):5139-49. doi: 10.4049/jimmunol.1401680. Epub 2015 Apr 20.