Miller William C, Wallace Stephanie, Kamm William, Reardon Erin, Theis-Mahon Nicole, Yousefzadeh Matthew J, Schmidt Elizabeth L, Niedernhofer Laura J, Puskarich Michael A
University of Minnesota Medical School, Minneapolis, MN, United States.
Department of Emergency Medicine, University of Minnesota and Hennepin Healthcare, Minneapolis, MN, United States.
Front Aging. 2024 Nov 15;5:1500741. doi: 10.3389/fragi.2024.1500741. eCollection 2024.
This systematic review explores the relationship between cellular senescence, an age-related inflammatory phenomenon, with acute human infectious disease.
Embase via OVID, Scopus, Web of Science, Global Index Medicus, Cochrane Library via Wiley, and ClinicalTrials.gov were queried. Included studies must have compared at least one of the following measures of cellular senescence between patients with an infection and without an infection: cell cycle inhibition measured via levels of and/or , short telomere length, DNA damage via ɣH2AX, high senescence-associated β galactosidase activity, and inflammation via the detection of senescence associated secretory phenotype (SASP). Manuscripts were screened and data collected via two independent reviewers.
A total of 15,828 studies were screened after duplicates were removed. One hundred and fifty-three full-text articles were assessed for eligibility and a total of 16 original articles were included in analysis. Of the 16 original articles included, 12 (75%) articles were centered on SARS-CoV-2, 2 (12.5%) articles utilized patients infected with , 1 (6.25%) with , and 1 (6.25%) with Hepatitis C.
Current literature demonstrates robust upregulation of markers of cellular senescence in the setting of acute SARS-CoV-2, , , and hepatitis C virus, and that markers of senescence correlate with disease severity and persist for months after resolution. Limitations in the number and types of infectious organisms studied, low sample sizes, modest longitudinal sampling, and a lack of consistency in markers measured, the method of measurement, and the definition of normal values represent ongoing gaps in the literature.
https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=421473, Identifier CRD42023421473.
本系统评价探讨细胞衰老(一种与年龄相关的炎症现象)与人类急性传染病之间的关系。
通过OVID检索Embase、Scopus、Web of Science、全球医学索引、通过Wiley检索Cochrane图书馆以及ClinicalTrials.gov。纳入的研究必须比较了感染患者和未感染患者之间以下至少一种细胞衰老指标:通过p16和/或p21水平测量的细胞周期抑制、短端粒长度、通过ɣH2AX检测的DNA损伤、高衰老相关β半乳糖苷酶活性以及通过检测衰老相关分泌表型(SASP)的炎症。稿件由两名独立审稿人进行筛选和数据收集。
去除重复项后共筛选了15828项研究。对153篇全文文章进行了资格评估,共有16篇原创文章纳入分析。在纳入的16篇原创文章中,12篇(75%)文章以严重急性呼吸综合征冠状病毒2(SARS-CoV-2)为中心,2篇(12.5%)文章研究了感染流感病毒的患者,1篇(6.25%)研究了感染登革热病毒的患者,1篇(6.25%)研究了感染丙型肝炎病毒的患者。
当前文献表明,在急性SARS-CoV-2、流感病毒、登革热病毒和丙型肝炎病毒感染情况下,细胞衰老标志物有显著上调,并且衰老标志物与疾病严重程度相关,在疾病缓解后仍持续数月。所研究的感染生物体的数量和类型、样本量小、纵向抽样有限以及所测量标志物、测量方法和正常值定义缺乏一致性等限制因素,代表了文献中存在的持续差距。
https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=421473,标识符CRD42023421473。