Table 1.
Outline of the pathways involved in the pro-regenerative effects of EVs in different tissues. PI3K: phosphatidylinositol-3-kinase; AKT: protein kinase B; WNT: wingless-related integration site; JNK: c-Jun N-terminal kinase; ATM: ATM serine/threonine kinase; IGF: insulin-related growth factor; HGF: hepatic growth factor; FGF: fibroblast growth factor; mTOR: mammalian target of rapamycin; RPTOR: regulatory-associated protein of mTOR; TGF-β: transforming growth factor β; CCL2: chemokine (C-C motif) ligand 2.
References | Tissue | Effect | Pathway Involved |
---|---|---|---|
[69] | Brain | Neuroprotective effect in ischemia and traumatic brain injury | Activation of PI3K/AKT pathway and calcium oscillations |
[70] | Brain | Decrease in neuronal apoptosis and motor recovery | Activation of Wnt/β-catenin signaling |
[71] | Heart | Enhanced myocardial viability in ischemia/reperfusion | Activation of PI3K/AKT pathway and reduced phosphorylated-c-JNK |
[10,72,73] | Endothelial cells | Improved angiogenesis | Activation of VEGF signaling and PI3K/AKT, repression of ATM |
[74] | Muscle | Prevention of muscle damage in hind limb ischemia | Activation of Neuregulin-1 |
[74] | Muscle | Improved myogenesis | Increased IGFs, HGFs and FGFs |
[75] | Muscle | Improved muscle regeneration in aging | Activation of Klotho pathway |
[76] | Bone | Decrease in radiation-induced bone loss | Activation of Wnt/β-catenin signaling |
[77] | Bone | Improved bone regeneration | Activation of AKT/mTOR pathway |
[78] | Lung | Amelioration of acute lung injury | Induction of RPTOR/mTOR pathway |
[79] | Lung | Antifibrotic effect in a model of pulmonary fibrosis | Inhibition of TGF-β-Wnt crosstalk |
[80] | Kidney | Decreased kidney injury in ischemia/reperfusion | Inhibition of CCL2 pathway |
[81] | Liver | Amelioration of hepatic ischemia/reperfusion injury | Inhibition of MEK/ERK pathway |