Table 3 Factors influencing stem cell therapy in NEC
From: Stem cell therapy as a promising strategy in necrotizing enterocolitis
Stem cell type | Intervention | Protection or risk | Key mechanisms | References |
|---|---|---|---|---|
ISCs | HB-EGF | Protection | Protect ISCs from injury by PI3K and EGFR/MEK1/2/ERK1/2 pathways | Chen et al. (2012) |
ISCs | Retinoic acid | Protection | Prevent apoptosis; protect ISCs by balancing pro-inflammatory Th17 and anti-inflammatory Tregs | Nino et al. (2017) |
ISCs | Exosomes from human milk | Protection | Protect ISCs from oxidative stress injury through Wnt/β-catenin signaling | Dong et al. (2020) |
ISCs | Corticotropin-releasing hormone receptor 2 | Protection | Enhance ISCs expression via phosphorylation of STAT3 and IL-22 | Li et al. (2017) |
ISCs | Combination of multiple stress factors | Risk | Diminish expression of LGR5+ ISCs | Lee et al. (2018) |
BM-MSCs | HB-EGF | Protection | Reduce apoptosis; promote migration and proliferation; facilitate MSCs engraftment and protect engrafted MSCs | Yang et al. (2012a) |
AF-MSCs | HB-EGF | Protection | Increase chemotaxis; protect AF-MSCs against hypoxia-induced apoptosis effectively | Watkins et al. (2012) |
NSCs | HB-EGF | Protection | Elevate enteric neuronal nitric oxide synthase levels; promote differentiation, migration, and proliferation of NSCs by epidermal growth factor receptor |