Table 1.

The characteristics and values of EVs in the pathogenesis of OA.

Mechanisms	Sources	Characteristics	Functions	Ref.
Angiogenesis	FLS	High expression of VEGF	Stimulate neovascularization leading to OA progression	[37]
Mechanical overload	Chondrocytes	Increased number and abnormal levels of MGP, TNAP and NPP1 proteins	Increase cartilage calcification	[38]
Increased inflammatory component	M1 macrophage	High expression of miR-1246	Transfer miR-1246 to chondrocytes and activate the Wnt/β-catenin pathway by inhibiting the expression of GSK3β and Axin2	[39]
	Chondrocytes	High expression of miR-449a-5p	Inhibit autophagy in LPS-induced macrophages by inhibiting ATG4B expression, and promote the production of mitoROS and mature IL-1β	[40]
	FLS	High expression of miR-142-5p and RUNX2	Accelerate IL-1β-induced apoptosis and cartilage matrix degradation by miR-142-5p/RUNX2 in chondrocytes	[41]
	Chondrocytes	High expression of circ-BRWD1 and miR-1277	Promote matrix degradation and cell apoptosis	[42]
	Chondrocytes	High expression of circ-001846 and miR-149-5p	Mediate chondrocyte injury through miR-149-5p/WNT5b	[43]
	Synovial fluid	Low expression of miR-193b-3p	Decrease inhibition of HDAC3 expression and promotion of H3 acetylation	[44]
	Chondrocytes	Carrying autophagy-associated tubulin 1A/1B LC3	Cause cartilage calcification and degradation	[45]
	Osteoclast	High expression of miR-214-3p	Affect osteoblast activity and bone formation	[46]
	Osteoblast	High expression of miR-210-5p	Inhibit the oxygen consumption rate of chondrocytes and trigger catabolic gene expression of chondrocytes	[47]
Cellular senescence	Senescent chondrocytes	High expression of miR-27b, −199a, −185	Inhibit cartilage homeostasis and upregulate inflammations	[48]
	Chondrocytes	High expression of connexin 43	Promote inflammation and regulate cell senescence	[49]
	Senescent MSCs	Low expression of miR-21-5p	Reduce immunotherapy function	[50]
	SnCs	High expression of NF-κB	Participate in multiple innate and adaptive immune responses to spread inflammation	[51]
	Muscle	High expression of miR-34a-5p	Induce senescence of bone marrow stem cells	[52]
	MSCs	High expression of aging markers and miR-118-3p;	Affect the function and behavior of MSC	[53]
		low expression of pluripotent markers
	Senescent endothelial cells	High expression of miR-31	Reduce osteogenesis by knocking down FZD3 mRNA	[54]
	Senescent bone marrow	High expression of miR-183-5p	Reduce cell proliferation and differentiation, promote oxidative stress, thus inhibiting the osteogenic activity of young MSCs	[55]
Metabolic alterations	Vascular endothelial cells	Low expression of autophagy and p21	Increase levels of ROS, thereby inducing apoptosis	[56]
	Chondrocytes	High expression of miR-449a-5p	Inhibit macrophage autophagy by miR-449a-5p/ATG4B, cause ROS production, increase IL-1β production and ultimately aggravating synovitis and cartilage erosion	[40]
	Oxidative stress-EVs	/	Activate Toll-like receptor 4 through synergy between 15-lipoxygenase and secreted PLA 2, resulting in aseptic inflammation	[57]