Table 3.

Some miRNAs with Implication in OA Restricted to 2018–2020

Type	Implication	Reference
miR-140	Promoting cartilage formation↑, inhibiting degeneration↓, role in chondrogenesis (MSCs)	[227]
miR-23b-3p	Promotes ECM degradation by activating p38 MAPK in chondrocytes and OA cartilage	[228]
lncRNA HOTAIR	Silencing inhibited Wnt/β-catenin pathway, declined synovial inflammation and synoviocyte proliferation, and promoted apoptosis in OA rats	[229]
miR-103a-3p	Upregulation: cell proliferation↑, apoptosis↓, inflammation↓, caspase-3↓, Poly(ADP-ribose)-Polymerase (PARP)↓, IL-1β↓, IL-6↓, IL-10↓ and TNF-α↓. High mobility group box 1 (HMGB1), an inflammatory mediator of OA, is a target of miR-103a-3p	[230]
miR-145 and miR-221	Upregulation of miR-145 and miR-221: proliferation of periosteal cells↑ and chondrogenic potential↑. Evidence in support for the use of patient-derived exosomes (from ASCs), for potential amelioration of OA	[193]
miR-136-5p	BM-MSC-derived exosomal miR-136-5p: chondrocyte migration↑ in vitro and cartilage degeneration↓ in vivo, OA pathology↓	[231]
miR-495	CircSERPINE2 could mediate TGFBR2 expression by binding with miR-495. As a conclusion, CircSERPINE2 attenuated IL-1β-caused apoptosis and ECM degradation of chondrocytes by regulating miR-495/TGFBR2 axis → new target for OA treatment.	[232]
miR-17-5p	OA cartilage and IL-1β-induced chondrocytes: miR-17-5p↓ Fucosyltransferase (FUT)1↑	[233]
miR-296-3p	CircCDH13 contributes to OA pathogenesis by acting as a sponge of miR-296-3p and regulating the miR-296-3p-PTEN pathway. Silencing of CircCDH13: chondrocyte apoptosis↓, ECM catabolism↓, anabolism↑, in vivo: alleviated OA.	[234]

Abbreviations: ASC, adipose tissue-derived mesenchymal stromal cells; FUT, Fucosyltransferase; HMGB1, High mobility group box 1; i.a., intraarticular; MAPK, MAP kinase; miR, microRNA; PARP, Poly(ADP-ribose)-Polymerase; TGFBR2, Transforming growth factor β receptor 2; Wnt, wingless and integration site-1.