Cell therapy can positively influence these changes through paracrine signaling, EV cargo, mitochondrial transfer, antioxidant effects, immune-metabolic reprogramming, angiogenesis, BBB stabilization and support of plasticity
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Molecular pathways documented in preclinical research include: (1) activation of nitric oxide (NO) synthesis via L-arginine/eNOS pathway, (2) transcriptional upregulation of VEGF-A and FGF-2 favouring angiogenesis, (3) modulation of the Egr-1 early transcription factor involved in fibroblast proliferation, (4) interaction with 5-HT2A and dopaminergic receptors in some behavioural models, (5) stabilisation of endothelial function via eNOS modulation and reduction of oxidative stress (8-OH-dG, MDA)
Regulation of the metabolite -ketoisovaleric acid (KMV) promoted cancer cell proliferation, invasion, and cell cycle progression, contributing to therapy resistance
Mechanisms of resistance to endocrine therapy in breast cancer: focus on signaling pathways, miRNAs and genetically based resistance
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