Reprint

Research of Pathogenesis and Novel Therapeutics in Arthritis 2.0

Edited by
May 2023
508 pages
  • ISBN978-3-0365-7592-6 (Hardback)
  • ISBN978-3-0365-7593-3 (PDF)

This book is a reprint of the Special Issue Research of Pathogenesis and Novel Therapeutics in Arthritis 2.0 that was published in

Biology & Life Sciences
Chemistry & Materials Science
Medicine & Pharmacology
Summary

Arthritis has a high prevalence globally and includes over 100 types, the most common of which are rheumatoid arthritis, osteoarthritis, psoriatic arthritis, and inflammatory arthritis. All types of arthritis share common features of the disease, including monocyte infiltration, inflammation, synovial swelling, pannus formation, stiffness in the joints, and articular cartilage destruction. The exact etiology of arthritis remains unclear, and no cure exists as of yet. Anti-inflammatory drugs (NSAIDs and corticosteroids) are commonly used in the treatment of arthritis. However, these drugs are associated with significant side effects, such as gastric bleeding and an increased risk of heart attack and other cardiovascular problems. It is therefore crucial that we continue to research the pathogenesis of arthritis and seek to discover novel modes of therapy. This reprint summarizes the themes of the 29 articles published in our Special Issue “Research of Pathogenesis and Novel Therapeutics in Arthritis 2.0”. This reprint details important novel research discoveries that contribute to our current understanding of arthritis.

Format
  • Hardback
License
© by the authors
Keywords
rheumatoid arthritis; exercise therapy; autoimmune disorder; treadmill running; exercise; articular cartilage; collagen-induced arthritis; pro-inflammatory cytokine; connexin 43; osteoporosis; rheumatoid arthritis; collagen-induced arthritis; microenvironment; inflammation; mesenchymal stem/stromal cells; bone injury; repair/regeneration; microparticles; joint inflammatory diseases; Wnt signaling; Dkk-1; biologics; rheumatoid arthritis; ankylosing spondylitis; axial spondyloarthritis; bone homeostasis; osteoarthritis; aging; PTOA; gene expression; RNA-seq; cartilage degeneration; scRNA-seq; chondrocytes; osteoarthritis; rheumatoid arthritis; animal model; pain; melatonin; rheumatoid arthritis; angiotensin II; arthritis; bone erosion; inflammation; tumor necrosis factor; renin-angiotensin system; angiotensin II type 1 receptor; psoriatic arthritis; osteoclastogenesis; miR-941; WNT16; rheumatoid arthritis; polymorphism; genetic predisposition; mutation; methotrexate; interleukin; targeted therapy; rheumatoid arthritis; interstitial lung disease; subclinical involvement; ACPA; pulmonary function testing; CPET; surfactant protein D; DLCO; HRCT; lymph node stromal cells; rheumatoid arthritis; tolerance; autoimmunity; citrullination; macrophages; PADI2; inflammatory cytokines; adhesion; apoptosis; L5; macrophage foam cell; CD11c expression; atherosclerosis; rheumatoid arthritis (RA); osteoarthritis; synovium; cytokines; HHV-7; PCR; ELISA; immunohistochemistry; adipocyte; infrapatellar fat pad; osteoarthritis; anterior cruciate ligament; inflammation; osteoarthritis; cartilage; synovium; whole transcriptome sequencing; biomarker; osteoarthritis; CRISPR/Cas9; miRNA; genome editing; autoimmune arthritis; Nkx2-3; B cell activation; Spondyloarthritis; ankylosing arthritis; psoriatic arthritis; interleukin-17; interleukin-23; osteoarthritis; PTOA; gene expression; RNA-seq; cartilage degeneration; tibial compression; gut microbiome; antibiotics; LPS; adults; juvenile; cytokines; immune; laser blood irradiation; low-level laser; systemic; naïve rheumatoid arthritis; CD4+ T-lymphocytes; methotrexate response; IFNγ, IL-17A; STAT expression; osteonecrosis; taurine; mitochondrial function; glucocorticoid; discoidin domain receptors 1 (Ddr1); osteoarthritis (OA); autophagy; apoptosis; terminal differentiation; rheumatoid arthritis (RA); Treg; Th17; gene expression; microRNA; transcriptional factor; rheumatoid arthritis; JAK/STAT; Janus kinase inhibitors; cardiovascular system; heart failure; thromboembolic; lipid profile disturbances; cytokines; arthritis; treatment; molecular mechanisms; biomarkers; inflammatory cytokines; prevention; collagen triple helix repeat containing 1; CTHRC1; rheumatoid arthritis; biomarker; bone erosion; cartilage destruction; fibroblast-like synoviocytes; Wnt signaling