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2
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本文引用的文献

1
NIH SenNet Consortium to map senescent cells throughout the human lifespan to understand physiological health.NIH SenNet 联盟绘制人类整个生命周期中的衰老细胞图谱,以了解生理健康状况。
Nat Aging. 2022 Dec;2(12):1090-1100. doi: 10.1038/s43587-022-00326-5. Epub 2022 Dec 20.
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SARS-CoV-2 infection induces DNA damage, through CHK1 degradation and impaired 53BP1 recruitment, and cellular senescence.SARS-CoV-2 感染通过 CHK1 降解和 53BP1 募集受损,诱导 DNA 损伤,并导致细胞衰老。
Nat Cell Biol. 2023 Apr;25(4):550-564. doi: 10.1038/s41556-023-01096-x. Epub 2023 Mar 9.
3
Controlling Inflammation Improves Aging Skeletal Muscle Health.控制炎症可改善衰老骨骼肌健康。
Exerc Sport Sci Rev. 2023 Apr 1;51(2):51-56. doi: 10.1249/JES.0000000000000313. Epub 2023 Feb 1.
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Hallmarks of aging: An expanding universe.衰老的特征:一个不断扩大的领域。
Cell. 2023 Jan 19;186(2):243-278. doi: 10.1016/j.cell.2022.11.001. Epub 2023 Jan 3.
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GZMK CD8 T effector memory cells are associated with CD15 neutrophil abundance in non-metastatic colorectal tumors and predict poor clinical outcome.GZMK CD8 T 效应记忆细胞与非转移性结直肠肿瘤中的 CD15 中性粒细胞丰度相关,并预测不良临床结局。
Nat Commun. 2022 Nov 8;13(1):6752. doi: 10.1038/s41467-022-34467-3.
6
Rejuvenation of the aged brain immune cell landscape in mice through p16-positive senescent cell clearance.通过清除 p16 阳性衰老细胞使年老小鼠大脑免疫细胞的年轻化。
Nat Commun. 2022 Sep 27;13(1):5671. doi: 10.1038/s41467-022-33226-8.
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Characterization of cellular senescence in aging skeletal muscle.衰老骨骼肌中细胞衰老的特征。
Nat Aging. 2022 Jul;2(7):601-615. doi: 10.1038/s43587-022-00250-8. Epub 2022 Jul 15.
8
Cellular senescence: a key therapeutic target in aging and diseases.细胞衰老:衰老和疾病的关键治疗靶点。
J Clin Invest. 2022 Aug 1;132(15). doi: 10.1172/JCI158450.
9
Granzyme K CD8 T cells form a core population in inflamed human tissue.颗粒酶 K+CD8+T 细胞构成人炎症组织内的核心细胞群。
Sci Transl Med. 2022 Jun 15;14(649):eabo0686. doi: 10.1126/scitranslmed.abo0686.
10
Skeletal muscle aging, cellular senescence, and senotherapeutics: Current knowledge and future directions.骨骼肌衰老、细胞衰老和衰老治疗学:当前的知识和未来的方向。
Mech Ageing Dev. 2021 Dec;200:111595. doi: 10.1016/j.mad.2021.111595. Epub 2021 Nov 3.

衰老与炎症:美国老年学学会和美国国家老龄化研究所联合主办研讨会综述。

Senescence and Inflammation: Summary of a Gerontological Society of America and National Institute on Aging-Sponsored Symposium.

机构信息

Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota, USA.

Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota, USA.

出版信息

J Gerontol A Biol Sci Med Sci. 2023 Oct 9;78(10):1733-1739. doi: 10.1093/gerona/glad120.

DOI:10.1093/gerona/glad120
PMID:37148367
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10562889/
Abstract

The National Institute on Aging sponsored a symposium at the Gerontological Society of America (GSA) annual meeting in Indianapolis, Indiana, to discuss recent discoveries related to senescent and inflammatory mechanisms in aging and disease. Consistent with the 2022 Biological Sciences GSA program led by Dr. Rozalyn Anderson, the symposium featured early-stage investigators and a leader in the field of geroscience research. Cell senescence and immune interactions coordinate homeostatic and protective programming throughout the life span. Dysfunctional communication in this exchange eventuates in inflammation-related compositional changes in aged tissues, including propagation of the senescence-associated secretory phenotype and accumulation of senescent and exhausted immune cells. Presentations in this symposium explored senescent and immune-related dysfunction in aging from diverse viewpoints and featured emerging cellular and molecular methods. A central takeaway from the event was that the use of new models and approaches, including single-cell -omics, novel mouse models, and 3D culture systems, is revealing dynamic properties and interactions of senescent and immune cell fates. This knowledge is critical for devising new therapeutic approaches with important translational relevance.

摘要

美国国家老龄化研究所(National Institute on Aging)在印第安纳州印第安纳波利斯举行的美国老年学学会(Gerontological Society of America,GSA)年会上主办了一次研讨会,讨论与衰老和疾病相关的衰老和炎症机制的最新发现。该研讨会与罗扎林·安德森博士(Rozalyn Anderson)领导的 2022 年生物科学 GSA 计划一致,特色是早期研究人员和衰老科学研究领域的领导者。细胞衰老和免疫相互作用协调整个生命周期的体内平衡和保护编程。这种交流中的功能障碍会导致衰老组织中与炎症相关的组成变化,包括衰老相关分泌表型的传播和衰老和耗竭免疫细胞的积累。本次研讨会从不同角度探讨了衰老过程中与衰老和免疫相关的功能障碍,并介绍了新兴的细胞和分子方法。该活动的一个重要收获是,新模型和方法的使用,包括单细胞组学、新型小鼠模型和 3D 培养系统,正在揭示衰老和免疫细胞命运的动态特性和相互作用。这些知识对于设计具有重要转化意义的新治疗方法至关重要。