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A rare idiopathic inflammatory myopathy (IIM) characterized principally by myositis, generally symmetrical arthritis and interstitial lung disease (ILD) in association with serum autoantibodies to aminoacyl-transfer RNA synthetases (anti-ARS). More variable features include arthralgia, Raynaud phenomenon, heliotrophic rash, distal esophageal dysmotility and mechanic's hands.
Selective JAK1/TYK2 inhibition blocks type I interferon receptor signaling, preventing STAT1/STAT2 phosphorylation and IRF9 complex formation. Reduces transcription of interferon-stimulated genes including IFIT1, ISG15, and MX1, while preserving JAK2/JAK3-dependent cytokine responses critical for immune surveillance.
Metformin activates AMPK through LKB1-dependent phosphorylation at Thr172, shifting T cell metabolism from glycolysis to oxidative phosphorylation. This metabolic switch preferentially impairs Th17 and Th1 effector function while promoting Foxp3+ regulatory T cell generation via mTORC1 inhibition and enhanced fatty acid oxidation.
Curcumin inhibits HDAC2 (histone deacetylase 2) activity, leading to increased acetylation of NF-κB p65 subunit, reducing its DNA binding affinity and suppressing transcription of pro-inflammatory cytokines IL-1β, TNF-α, and IL-6. Additionally modulates macrophage polarization from M1 to M2 phenotype via STAT6 pathway activation.
Baicalin (from Scutellaria baicalensis) promotes Nrf2 nuclear translocation by disrupting Keap1-Nrf2 interaction. Activated Nrf2 upregulates antioxidant response elements including HO-1, NQO1, and GCLM. Simultaneously inhibits TGF-β1-induced myofibroblast differentiation by suppressing Smad2/3 phosphorylation and α-SMA expression.
Rituximab depletes CD20+ B cells reducing autoantibody production against aminoacyl-tRNA synthetases. Low-dose naltrexone (1.5-4.5mg) acts as TLR4 antagonist on microglia and muscle-resident macrophages, reducing MyD88-dependent signaling cascade and decreasing IL-1β, IL-18 production via NLRP3 inflammasome inhibition.
Inhibition of ACSL4 (acyl-CoA synthetase long-chain family member 4) reduces arachidonic acid incorporation into phospholipids, decreasing lipid peroxidation and ferroptotic cell death. Simultaneously upregulates GPX4 and System Xc- (SLC7A11) to enhance glutathione-dependent lipid peroxide clearance in muscle fibers.
Bacosides from Brahmi extract antagonize C5aR1 (CD88) receptor on microglia and astrocytes, preventing C5a-induced calcium influx and subsequent NLRP3 inflammasome activation. Reduces complement-mediated neuromuscular junction inflammation and preserves acetylcholine receptor clustering via agrin-LRP4-MuSK pathway protection.