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1
Murine mesenchymal cells that express elevated levels of the CDK inhibitor p16(Ink4a) in vivo are not necessarily senescent.体内表达高水平细胞周期蛋白依赖性激酶抑制剂p16（Ink4a）的小鼠间充质细胞不一定衰老。
Cell Cycle. 2017 Aug 18;16(16):1526-1533. doi: 10.1080/15384101.2017.1339850. Epub 2017 Jun 26.
2
p16(Ink4a) and senescence-associated β-galactosidase can be induced in macrophages as part of a reversible response to physiological stimuli.p16（Ink4a）和衰老相关β半乳糖苷酶可在巨噬细胞中被诱导产生，作为对生理刺激的可逆反应的一部分。
Aging (Albany NY). 2017 Aug 2;9(8):1867-1884. doi: 10.18632/aging.101268.
3
Aging of mice is associated with p16(Ink4a)- and β-galactosidase-positive macrophage accumulation that can be induced in young mice by senescent cells.小鼠衰老与p16（Ink4a）和β-半乳糖苷酶阳性巨噬细胞的积累有关，衰老细胞可在年轻小鼠中诱导这种积累。
Aging (Albany NY). 2016 Jul;8(7):1294-315. doi: 10.18632/aging.100991.
4
Cells exhibiting strong promoter activation in vivo display features of senescence.体内具有强烈启动子激活的细胞表现出衰老的特征。
Proc Natl Acad Sci U S A. 2019 Feb 12;116(7):2603-2611. doi: 10.1073/pnas.1818313116. Epub 2019 Jan 25.
5
p16-expressing mesenchymal stromal cells restore the senescence-clearance-regeneration sequence that is impaired in chronic muscle inflammation.表达 p16 的间充质基质细胞恢复了慢性肌肉炎症中受损的衰老清除-再生序列。
EBioMedicine. 2019 Jun;44:86-97. doi: 10.1016/j.ebiom.2019.05.012. Epub 2019 May 23.
6
Cellular Senescence in Diabetes Mellitus: Distinct Senotherapeutic Strategies for Adipose Tissue and Pancreatic β Cells.糖尿病中的细胞衰老：脂肪组织和胰腺 β 细胞的独特衰老治疗策略。
Front Endocrinol (Lausanne). 2022 Mar 31;13:869414. doi: 10.3389/fendo.2022.869414. eCollection 2022.
7
Tumor suppressor and aging biomarker p16(INK4a) induces cellular senescence without the associated inflammatory secretory phenotype.肿瘤抑制因子和衰老生物标志物 p16(INK4a) 在没有相关炎症分泌表型的情况下诱导细胞衰老。
J Biol Chem. 2011 Oct 21;286(42):36396-403. doi: 10.1074/jbc.M111.257071. Epub 2011 Aug 31.
8
Mesenchymal stem cell senescence alleviates their intrinsic and seno-suppressive paracrine properties contributing to osteoarthritis development.间充质干细胞衰老减轻了它们固有的和抑制衰老的旁分泌特性，从而促进骨关节炎的发展。
Aging (Albany NY). 2019 Oct 22;11(20):9128-9146. doi: 10.18632/aging.102379.
9
H3K9me-enhanced DNA hypermethylation of the p16INK4a gene: an epigenetic signature for spontaneous transformation of rat mesenchymal stem cells.H3K9me 增强的 p16INK4a 基因 DNA 超甲基化：大鼠间充质干细胞自发转化的表观遗传标志。
Stem Cells Dev. 2013 Jan 15;22(2):256-67. doi: 10.1089/scd.2012.0172. Epub 2012 Nov 7.
10
Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders.清除 p16Ink4a 阳性衰老细胞可延缓与衰老相关的疾病。
Nature. 2011 Nov 2;479(7372):232-6. doi: 10.1038/nature10600.

引用本文的文献

1
Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.应对成骨细胞衰老：分子途径与抗衰老治疗前沿
Clin Transl Med. 2025 Jul;15(7):e70417. doi: 10.1002/ctm2.70417.
2
Multi-omics analysis of canine aging markers and evaluation of stem cell intervention.犬类衰老标志物的多组学分析及干细胞干预评估
Commun Biol. 2025 Jun 10;8(1):905. doi: 10.1038/s42003-025-08333-z.
3
The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.衰老、昼夜节律和癌症的共同特征及相互关联途径：对治疗策略的启示
Research (Wash D C). 2025 Mar 5;8:0612. doi: 10.34133/research.0612. eCollection 2025.
4
The potential for senotherapy as a novel approach to extend life quality in veterinary medicine.衰老疗法作为一种在兽医学中延长生命质量的新方法的潜力。
Front Vet Sci. 2024 May 15;11:1369153. doi: 10.3389/fvets.2024.1369153. eCollection 2024.
5
Cellular senescence and kidney aging.细胞衰老与肾脏老化。
Clin Sci (Lond). 2023 Dec 22;137(24):1805-1821. doi: 10.1042/CS20230140.
6
Senescent Microglia Represent a Subset of Disease-Associated Microglia in P301S Mice.衰老的小胶质细胞代表 P301S 小鼠中与疾病相关的小胶质细胞的一个亚群。
J Alzheimers Dis. 2023;95(2):493-507. doi: 10.3233/JAD-230109.
7
Multiparametric senescent cell phenotyping reveals targets of senolytic therapy in the aged murine skeleton.多参数衰老细胞表型分析揭示衰老治疗在老年鼠骨骼中的靶点。
Nat Commun. 2023 Jul 31;14(1):4587. doi: 10.1038/s41467-023-40393-9.
8
The ageing immune system as a potential target of senolytics.衰老的免疫系统作为衰老细胞溶解剂的潜在靶点。
Oxf Open Immunol. 2023 May 3;4(1):iqad004. doi: 10.1093/oxfimm/iqad004. eCollection 2023.
9
Multiparametric senescent cell phenotyping reveals CD24 osteolineage cells as targets of senolytic therapy in the aged murine skeleton.多参数衰老细胞表型分析揭示CD24骨系细胞是老年小鼠骨骼中衰老细胞溶解疗法的靶点。
bioRxiv. 2023 Jan 13:2023.01.12.523760. doi: 10.1101/2023.01.12.523760.
10
P16INK4A-More Than a Senescence Marker.P16INK4A——不止是一个衰老标志物。
Life (Basel). 2022 Aug 28;12(9):1332. doi: 10.3390/life12091332.

本文引用的文献

1
Senescent cells expose and secrete an oxidized form of membrane-bound vimentin as revealed by a natural polyreactive antibody.一种天然多反应性抗体显示，衰老细胞会暴露并分泌一种膜结合波形蛋白的氧化形式。
Proc Natl Acad Sci U S A. 2017 Feb 28;114(9):E1668-E1677. doi: 10.1073/pnas.1614661114. Epub 2017 Feb 13.
2
Aging of mice is associated with p16(Ink4a)- and β-galactosidase-positive macrophage accumulation that can be induced in young mice by senescent cells.小鼠衰老与p16（Ink4a）和β-半乳糖苷酶阳性巨噬细胞的积累有关，衰老细胞可在年轻小鼠中诱导这种积累。
Aging (Albany NY). 2016 Jul;8(7):1294-315. doi: 10.18632/aging.100991.
3
Naturally occurring p16(Ink4a)-positive cells shorten healthy lifespan.天然存在的p16（Ink4a）阳性细胞会缩短健康寿命。
Nature. 2016 Feb 11;530(7589):184-9. doi: 10.1038/nature16932. Epub 2016 Feb 3.
4
Clearance of senescent cells by ABT263 rejuvenates aged hematopoietic stem cells in mice.ABT263清除衰老细胞可使小鼠体内衰老的造血干细胞恢复活力。
Nat Med. 2016 Jan;22(1):78-83. doi: 10.1038/nm.4010. Epub 2015 Dec 14.
5
Forging a signature of in vivo senescence.伪造体内衰老的签名。
Nat Rev Cancer. 2015 Jul;15(7):397-408. doi: 10.1038/nrc3960.
6
Size- and shape-dependent foreign body immune response to materials implanted in rodents and non-human primates.植入啮齿动物和非人灵长类动物体内的材料的尺寸和形状依赖性异物免疫反应。
Nat Mater. 2015 Jun;14(6):643-51. doi: 10.1038/nmat4290. Epub 2015 May 18.
7
Senescence and apoptosis: dueling or complementary cell fates?衰老与凋亡：相互对抗还是相互补充的细胞命运？
EMBO Rep. 2014 Nov;15(11):1139-53. doi: 10.15252/embr.201439245. Epub 2014 Oct 13.
8
p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes.p53 依赖性 HMGB1 警报素的释放是衰老表型的核心介质。
J Cell Biol. 2013 May 13;201(4):613-29. doi: 10.1083/jcb.201206006. Epub 2013 May 6.
9
Monitoring tumorigenesis and senescence in vivo with a p16(INK4a)-luciferase model.利用 p16(INK4a)-荧光素酶模型在体内监测肿瘤发生和衰老。
Cell. 2013 Jan 17;152(1-2):340-51. doi: 10.1016/j.cell.2012.12.010.
10
Ionizing radiation-induced expression of INK4a/ARF in murine bone marrow-derived stromal cell populations interferes with bone marrow homeostasis.电离辐射诱导 INK4a/ARF 在小鼠骨髓基质细胞群体中的表达会干扰骨髓内稳态。
Blood. 2012 Jan 19;119(3):717-26. doi: 10.1182/blood-2011-06-361626. Epub 2011 Nov 18.

体内表达高水平细胞周期蛋白依赖性激酶抑制剂p16（Ink4a）的小鼠间充质细胞不一定衰老。

Murine mesenchymal cells that express elevated levels of the CDK inhibitor p16(Ink4a) in vivo are not necessarily senescent.

作者信息

Frescas David, Hall Brandon M, Strom Evguenia, Virtuoso Lauren P, Gupta Mahima, Gleiberman Anatoli S, Rydkina Elena, Balan Vitaly, Vujcic Slavoljub, Chernova Olga B, Gudkov Andrei V

机构信息

a Everon Biosciences, Inc. , Buffalo , NY , USA.

b Dept. of Cell Stress Biology , Roswell Park Cancer Institute , Buffalo , NY , USA.

出版信息

Cell Cycle. 2017 Aug 18;16(16):1526-1533. doi: 10.1080/15384101.2017.1339850. Epub 2017 Jun 26.

DOI:10.1080/15384101.2017.1339850
PMID:28650766
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5584871/
Abstract

Age-related health decline has been attributed to the accumulation of senescent cells recognized in vivo by p16(Ink4a) expression. The pharmacological elimination of p16(Ink4a)-positive cells from the tissues of mice was shown to extend a healthy lifespan. Here, we describe a population of mesenchymal cells isolated from mice that are highly p16(INK4a)-positive are proficient in proliferation but lack other properties of cellular senescence. These data, along with earlier reports on p16(Ink4a)-positive macrophages, indicate that p16(Ink4a)-positive and senescent cell populations only partially intersect, therefore, extending the list of potential cellular targets for anti- aging therapies.

摘要

与年龄相关的健康衰退被归因于通过p16(Ink4a)表达在体内识别出的衰老细胞的积累。从小鼠组织中通过药理学方法清除p16(Ink4a)阳性细胞可延长健康寿命。在此，我们描述了从老鼠体内分离出的一群间充质细胞，这些细胞高度p16(INK4a)阳性，具有旺盛的增殖能力，但缺乏细胞衰老的其他特征。这些数据，连同早期关于p16(Ink4a)阳性巨噬细胞的报道，表明p16(Ink4a)阳性细胞群和衰老细胞群只是部分重叠，因此，扩展了抗衰老疗法潜在细胞靶点的清单。