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Abstract
Rheumatoid arthritis is categorized as a systematic autoimmune disease which causes chronic disabilities exclusively in bones that are aligned with synovium. RA aetiology is still unknown but previous studies have coined that several number of factors play a significant role e.g. environmental and genetic factors. Cellular signalling pathways orchestrate the inflammatory response that regulates various cellular functions like cellular progression, proliferation, death and secretion of signalling molecules (pro and anti-inflammatory cytokines) in response to genetic and environmental stimuli. These regulatory pathways are tightly controlled Rheumatoid arthritis is categorized as a systematic autoimmune disease which causes chronic disabilities exclusively in bones that are aligned with synovium. RA aetiology is still unknown but previous studies have coined that several number of factors play a significant role e.g. environmental and genetic factors. Cellular signalling pathways orchestrate the inflammatory response that regulates various cellular functions like cellular progression, proliferation, death and secretion of signalling molecules (pro and anti-inflammatory cytokines) in response to genetic and environmental stimuli. These regulatory pathways are tightly controlled and naturally activated by ligands that attach to their respective receptors on the cell surface. In diseased state, these signalling pathways escape the normal control mechanisms, resulting in intensification of cytokines and chemokines, transcription factors and mediatory proteins that disrupt normal cell processes and might bring about auto-destructive consequences such as in the case of rheumatoid arthritis. The review highlights multiple levels of targeting molecules in signalling pathways that may be potential diagnostic markers and also attempts to underline potential therapeutic targets.and naturally activated by ligands that attach to their respective receptors on the cell surface. In diseased state, these signalling pathways escape the normal control mechanisms, resulting in intensification of cytokines and chemokines, transcription factors and mediatory proteins that disrupt normal cell processes and might bring about auto-destructive consequences such as in the case of rheumatoid arthritis. The review highlights multiple levels of targeting molecules in signalling pathways that may be potential diagnostic markers and also attempts to underline potential therapeutic targets.
Highlights
Rheumatoid arthritis (RA) is a chronic autoimmune disease, characterized by inflammation of joints especially small joints of hands and feet leading to joints deformation and bone destruction
This review highlights various signalling pathways involved in pathogenesis of RA e.g. MAPK pathway, Wnt signalling pathway, Janus kinase (JAK)/Signal transducers and activators of transcription (STATs) pathway, NFκB signalling and toll-like receptors (TLRs) signalling, their activation, function, role in regulating cytokines and promoting inflammation and subsequent tissue destruction and aims to summarize potential therapeutic targets identified so far in order to provide an efficient therapy for the disease
Cellular responses are assimilated to environmental stresses by a group of signal transducing enzymes known as mitogenactivated protein kinases abbreviated as MAPKs(Inoue et al, 2006)
Summary
Rheumatoid arthritis (RA) is a chronic autoimmune disease, characterized by inflammation of joints especially small joints of hands and feet leading to joints deformation and bone destruction. It involves imbalances in pro-inflammatory and anti-inflammatory cytokines levels (Paunovic & Harnett, 2013). The signalling pathways of these inflammatory cytokines have emerged to have promising potential to be targeted by well-defined therapies thereby inhibiting inflammation and disease pathogenesis (Schett, 2011). Depending on the progressive autoimmune nature, certain complexities are linked within a number of organ systems, which worsens the condition The basis for such chronic inflammatory processes are sustained communication networks between cells within a tissue type and between different tissues. This review highlights various signalling pathways involved in pathogenesis of RA e.g. MAPK pathway, Wnt signalling pathway, JAK/STAT pathway, NFκB signalling and TLR signalling, their activation, function, role in regulating cytokines and promoting inflammation and subsequent tissue destruction and aims to summarize potential therapeutic targets identified so far in order to provide an efficient therapy for the disease
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