时间标签:数据日期 2026-10-31 · 生成时间 2026-11-01 05:30(Asia/Shanghai)| 检索窗口 PubMed edat 2026/10/28–2026/10/31 | 情报发生日期 2026-10-31
研究问题
This model asks whether age‐dependent MSC signaling, particularly altered chemokine synthesis, helps explain regenerative decline across stem cell systems.;However, lineage tracing shows that pericytes in several organs do not broadly generate tissue‐specific mesenchymal lineages during homeostasis, limiting their general classification as MSCs (Guimarães‐Camboa et al. ).
方法
Putative MSCs are identified by tissue‐specific localization, surface markers, lineage tracing, and functional assays.;Following myocardial injury, these cells are activated and recruited to sites of damage through mechanisms that include CXCL12‐CXCR4 signaling (Zhuang et al. ).;Aged hair follicle stem cells also display reduced niche mobilization and regenerative potential in transplantation assays, which may reflect altered chemokine gradients or responsiveness as contributing factors (Ge et al. ).
核心结论
Over a lifetime, higher organisms sustain continuous biochemical, molecular, and cellular damage.;Once expanded ex vivo, human MSCs are defined by plastic adherence, CD73, CD90, and CD105 expression, absence of CD45, CD34, CD14 or CD11b, CD79α or CD19, and HLA‐DR, and osteogenic, adipogenic, and chondrogenic differentiation in vitro (Dominici et al. ).;Throughout this review, “MSC” therefore denotes tissue‐resident mesenchymal stromal populations with reported MSC‐like phenotypes or functions, without implying a common developmental origin, marker profile, or multipotency. ‖ 结论:Collectively, the evidence positions dysregulated chemokine synthesis by tissue‐resident MSCs as a mechanistic interface between cellular aging, chronic inflammation, and stem cell decline, while identifying restoration of MSC signaling fidelity as a potential strategy to preserve regenerative capacity during aging.
局限
Future studies must therefore distinguish chemokines associated with MSC aging from those that are necessary or sufficient to drive stem cell dysfunction and determine whether their normalization restores regenerative function in vivo.
对本项目的价值
★★☆☆☆ 细胞衰老清除/重编程是项目干预管线的核心支柱之一。
全文来源
PMC JATS 全文(正文 51,996 字符,已过标题/DOI 逐字归属校验)
原文题录
- 英文标题:Senescent Mesenchymal Stromal Cells Drive Stem Cell Aging Through Dysregulated Chemokine Synthesis.
- 期刊与标识:Aging Cell · PMID 42951861 · DOI 10.1111/acel.70780
C 级证据分级:C 级(预印本 / 观点评论,非原始研究)
本文属观点/评论类文献,不是原始研究。其论点依赖于作者对既有证据的梳理与判断,不构成新的实验证据。本站标注 C 级即为此意——阅读时请把它当作「领域内的思考框架」,而非「研究发现」。
关于本文的文献来源:本站依据 IMA 知识库「五刊监控·深度文献卡片」撰写,依据已获取的期刊全文(方法、样本量与结论已回到原文核对);未能获取全文的同批条目另行标注「摘要级」,全程未做任何数值推算补全。