Advances in research of neutrophil extracellular trap formation in osteoarticular diseases

Table 1 Role and mechanism of neutrophil extracellular traps in different osteoarticular diseases

Ref.	Disease	Mechanism	Role of NETs	Species
Schneider et al[55]	RA	NETs/TLR/RANKL/osteoclastogenesis	Bone erosion	Mouse/cell
Carmona et al[54]	RA	NETs/NE/PAD2/CD4+ T cells	Cartilage damage and synovial inflammation	Mouse/cell
Song et al[53]	RA	ACPA	Autoimmune diseases	Human/mouse/cell
Papagoras et al[61]	AS	IL-1β/IL-17/NETs/MSCs/bone-forming cells	Inflammation and neoosteogenesis	Mouse/cell
Maueröder et al[67]	Gout	MSU/NLRP3/ IL- 1β/NETs	Inflammation	Mouse/cell
Luan et al[72]	OA	TLR7/MAPK/NETs	Cartilage and bone damage	Human/mouse/cell
Nonokawa et al[77]	ONFH	Activated platelets/NETs	Microangiopathy	Human/rat
Jin et al[83]	Fibrosis	HMGB1/NETs/RAGE (macrophages)/NF-κb/Smad3	Increased α-SMA and fibronectin expression	Mouse

NETs: Neutrophil extracellular traps; RA: Rheumatoid arthritis; TLR: Toll-like receptor 2; RANKL: Receptor activator of nuclear factor kappa-B ligand; NE: Neutrophil elastase; PAD: Peptidyl arginine deiminases; ACPA: Anti-citrullinated protein antibody; AS: Ankylosing spondylitis; OA: Osteoarthritis; ONFH:; MSCs: Mesenchymal stem cells; IL: Interleukin; NLRP3: Nucleotide-binding domain, leucine-rich repeat and pyrin domain-containing protein 3; MSU: Monosodium urate; MAPK: Mitogen-activated protein kinase; α-SMA: Alpha-smooth muscle actin; HMGB1: High mobility group box 1; NF-κb: Nuclear factor kappa-B.