Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Apr 6;13:31. doi: 10.1186/s13045-020-00864-8

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

PMC Copyright notice

Fig. 1 — Functional alterations and HSC aging mechanisms. Aging negatively affects HSC functions, including decreasing self-renewal ability and myeloid/platelet-biased differentiation and impairing implantation ability. The intrinsic mechanisms are illustrated at the gene level, signaling pathway level, and epigenetic level. HSC aging is accompanied by some cell surface markers being upregulated with age (such as CD28, CD38, CD41, CD47, CD62, CD 69, CD74, and CD81) and some being downregulated with age (such as CD27, CD34, CD37, CD44, CD48, CD52, CD63, CD79b, CD86, CD97, CD97b, and CD160). Furthermore, aged HSCs show different expression levels of specific genes. For example, Amp3, Anxa7, Ap3b1, SELP, Egr1, Arhgef12, and Cbfa2t1h are upregulated, and Flt3, Xab2, Rad52, Xrcc1, Sox17, Bcl11b, and Blnk are downregulated. In addition, some signaling pathways are activated/repressed during HSC aging, including the JAK/STAT-NF-κB-mTOR pathway, TGF-β pathway, Wnt pathway, and ROS and UPR^mt pathway. Age-related epigenetic regulation includes DNMT1, DNMT3A, DNMT3B, H3K4me3, and H3K27me3. Extrinsic mechanisms include HSC-surrounding cells (including MSCs, neutrophils, megakaryocytes, and macrophages), cytokines (including IL-6 and IL-1B), enzymes (including caspase-1), and β-adrenergic nerve signaling (including increased β2-AR signaling and decreased β3-AR signaling). The red box indicates that the molecule is upregulated with age, and the green box indicates that the molecule is downregulated with age