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Research of Pathogenesis and Novel Therapeutics in Arthritis 2.0
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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.
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Keywords
- ACPA
- Adhesion
- adipocyte
- adults
- Aging
- Angiotensin II
- angiotensin II type 1 receptor
- animal model
- ankylosing arthritis
- ankylosing spondylitis
- anterior cruciate ligament
- antibiotics
- Apoptosis
- Arthritis
- articular cartilage
- Atherosclerosis
- autoimmune arthritis
- autoimmune disorder
- Autoimmunity
- Autophagy
- Axial spondyloarthritis
- B cell activation
- biologics
- biomarker
- biomarkers
- bone erosion
- bone homeostasis
- bone injury
- Cardiovascular system
- cartilage
- cartilage degeneration
- cartilage destruction
- CD11c expression
- CD4+ T-lymphocytes
- chondrocytes
- citrullination
- collagen triple helix repeat containing 1
- collagen-induced arthritis
- connexin 43
- CPET
- CRISPR/Cas9
- CTHRC1
- Cytokines
- discoidin domain receptors 1 (Ddr1)
- Dkk-1
- DLCO
- ELISA
- Exercise
- Exercise therapy
- fibroblast-like synoviocytes
- Gene expression
- genetic predisposition
- Genome editing
- glucocorticoid
- gut microbiome
- Heart Failure
- HHV-7
- HRCT
- IFNγ, IL-17A
- immune
- immunohistochemistry
- Inflammation
- inflammatory cytokines
- infrapatellar fat pad
- interleukin
- interleukin-17
- interleukin-23
- interstitial lung disease
- JAK/STAT
- Janus kinase inhibitors
- joint inflammatory diseases
- Juvenile
- L5
- laser blood irradiation
- lipid profile disturbances
- low-level laser
- LPS
- lymph node stromal cells
- macrophage foam cell
- Macrophages
- medicine
- Melatonin
- mesenchymal stem/stromal cells
- methotrexate
- methotrexate response
- microenvironment
- microparticles
- microRNA
- miR-941
- miRNA
- mitochondrial function
- molecular mechanisms
- Mutation
- naïve rheumatoid arthritis
- Nkx2-3
- Osteoarthritis
- osteoarthritis (OA)
- osteoclastogenesis
- osteonecrosis
- osteoporosis
- Other branches of medicine
- PADI2
- Pain
- PCR
- Pharmacology
- polymorphism
- Prevention
- pro-inflammatory cytokine
- psoriatic arthritis
- PTOA
- pulmonary function testing
- renin-angiotensin system
- repair/regeneration
- Rheumatoid arthritis
- rheumatoid arthritis (RA)
- RNA-Seq
- scRNA-seq
- spondyloarthritis
- STAT expression
- subclinical involvement
- surfactant protein D
- synovium
- systemic
- targeted therapy
- Taurine
- terminal differentiation
- Th17
- thromboembolic
- tibial compression
- tolerance
- transcriptional factor
- treadmill running
- Treatment
- Treg
- tumor necrosis factor
- whole transcriptome sequencing
- Wnt signaling
- WNT16
Links
DOI: 10.3390/books978-3-0365-7593-3Editions