Lu S.H., et al. 2018 |
- |
Deficient or decreased expression of CD106 + MSCs accelerates bone marrow vascularization failure in AA patients |
Deng S., et al. 2019 |
- |
The activation of VEGF–Notch pathway can restore the proliferation function of MSCs in AA patients |
Li N., et al. 2020 |
3 |
The microRNA miR-144-3p is involved in AA pathogenesis. Its targeting may be a therapeutic strategy |
Li H., et al. 2017 |
15 |
Bone marrow-derived MSCs modulate the levels of T-helper (Th)1, Th2, Th17, and T-regulatory cells, as well as their related cytokines in AA patients |
Zhao J., et al. 2019 |
- |
Gingival-derived MSCs markedly improved survival and attenuated histological bone marrow damage in AA murine models |
Li J., et al. 2012 |
- |
MSCs from AA patients show differential gene expression profiles associated with bone marrow failure |
Huo J., et al. 2020 |
49 |
MSCs from AA patients exhibited multifaceted defects in biological characteristics and alterative molecular genetics in the whole genome |
Bueno C., et al. 2014 |
- |
MSC cultures from the bone marrow of AA patients display the same phenotype and differentiation potential as their counterparts from normal controls |