Table 1.

Molecular mechanisms and therapeutic potential of exosomal ncRNAs involved in diabetic wound healing.

Exo-ncRNAs	Molecular mechanisms	Final effect	Ref.
miR-223	Regulate macrophage polarization by targeting pknox1	Reduce inflammatory response	(11)
miR-let-7b	convert the polarization of macrophage via TLR4/NF-κB/STAT3/AKT signaling pathways	Reduce inflammatory response	(28)
miR-135a	Inhibit E-cadherin, N-cadherin, and LATS2 and promote α-SMA expression	Promote fibroblasts migration	(33)
miR-146a	Upregulate SERPIN and p-ERK2 expression in fibroblasts	Promote fibroblasts migration	(29)
miR-221-3p	Increase the expression of VEGF, CD31, and Ki67 involved in AGE-RAGE and p53 signaling pathway, cell cycle	Promote vascular cells proliferation	(38)
miR-126	activate the PI3K/AKT signaling pathway via miR-126-mediated PTEN downregulation	Promote angiogenesis	(30)
miR-21、-23a、-125b、-145	Inhibit TGF-b2, TGF-bR2, and SMAD2 and suppress α-SMA and collagen I expression	Anti-scarring effect	(31)
lncRNA-H19	Impair miR-152-3p-mediated PTEN inhibition	Inhibit apoptosis and inflammation, promote fibroblasts migration	(52)
lncRNA KLF3-AS1	Decrease miR-383 expression and upregulate VEGFA	Increase angiogenesis, reduced inflammation	(56)
lncRNA NEAT1	mediate Wnt/β-catenin signaling pathway	Increase angiogenesis	(51)
circKlhl8	Activate miR-212-3p/SIRT5 signaling pathway	Increase survival and maintain endothelial function in EPCs	(71)
mmu circ 0000250	Induce miR-128-3p/SIRT1 mediated autophagy	Increase angiogenesis and autophagy	(72)