Matrix Metalloproteinase Gene Activation Resulting from Disordred Epigenetic Mechanisms in Rheumatoid Arthritis.

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Term Occurence Count Dictionary
adalimumab 1 rheumatologydiseasesdrugs
anakinra 1 rheumatologydiseasesdrugs
infliximab 1 rheumatologydiseasesdrugs
rituximab 1 rheumatologydiseasesdrugs
tocilizumab 1 rheumatologydiseasesdrugs
arthritis 11 rheumatologydiseases
golimumab 1 rheumatologydiseasesdrugs
rheumatoid arthritis 1 rheumatologydiseases
tofacitinib 1 rheumatologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
adalimumab 7634 (1) TNF-α inhibition (infliximab [[32],[33],[34],[35]], etanercept [[36],[37],[38],[39],[40],[41]], adalimumab [[42],[43],[44]], golimumab [[45],[46],[47],[48],[49]], and certolizumab pegol [[50]]) [[51],[52],[53]];
anakinra 7902 disruption of T cell co-stimulation (abatacept [[56],[57],[58],[59],[60],[61]]); (4) IL-1 inhibition ( anakinra [[62]]); and (5) IL-6 inhibition (tocilizumab [[63],[64],[65],[66],[67],[68]]). The remainder of RA
golimumab 7663 (infliximab [[32],[33],[34],[35]], etanercept [[36],[37],[38],[39],[40],[41]], adalimumab [[42],[43],[44]], golimumab [[45],[46],[47],[48],[49]], and certolizumab pegol [[50]]) [[51],[52],[53]]; (2) B cell depletion (rituximab
infliximab 7556 RA patients successfully on average. They work via the following mechanisms: (1) TNF-α inhibition ( infliximab [[32],[33],[34],[35]], etanercept [[36],[37],[38],[39],[40],[41]], adalimumab [[42],[43],[44]], golimumab
rituximab 7772 [[45],[46],[47],[48],[49]], and certolizumab pegol [[50]]) [[51],[52],[53]]; (2) B cell depletion ( rituximab [[54],[55]]); (3) disruption of T cell co-stimulation (abatacept [[56],[57],[58],[59],[60],[61]]); (4)
tocilizumab 7945 (abatacept [[56],[57],[58],[59],[60],[61]]); (4) IL-1 inhibition (anakinra [[62]]); and (5) IL-6 inhibition ( tocilizumab [[63],[64],[65],[66],[67],[68]]). The remainder of RA patients do not respond or do not fully benefit
tofacitinib 8126 respond or do not fully benefit from these treatments. The therapeutic effect of the JAK inhibitor tofacitinib is similar to these antirheumatic biologics [[69],[70],[71],[72],[73]].The pathogenesis of RA is multifactorial
Select Disease Character Offset Disease Term Instance
arthritis 673 metalloproteinases (MMPs) are implicated in the degradation of extracellular matrix (ECM). Rheumatoid arthritis (RA) synovial fibroblasts (SFs) produce matrix-degrading enzymes, including MMPs, which facilitate cartilage
arthritis 2900 metalloproteinases (MMPs), which are involved in the pathogenesis of numerous diseases, such as rheumatoid arthritis (RA).The mechanisms regulating MMP transcription have been clarified. Pro-inflammatory cytokines, including
arthritis 11704 inhibitory antibody suppresses both cartilage destruction and disease progression in a collagen-induced arthritis (CIA) mouse model [[108]].Several studies have focused on the phenotype of MMP-deficient mice. MMP-8-deficient
arthritis 11929 have been backcrossed onto a Fas-defective MRL/lpr background that is characterized by spontaneous arthritis [[109]]. The mice showed earlier and more severe arthritis as well as an increase in neutrophil infiltration
arthritis 11988 background that is characterized by spontaneous arthritis [[109]]. The mice showed earlier and more severe arthritis as well as an increase in neutrophil infiltration due to delayed apoptosis. Therefore, MMP-8 is considered
arthritis 12245 whether gelatinases (MMP-2 and MMP-9) play an important role in RA, the development of antibody-induced arthritis in MMP-2 or MMP-9-deficient mice has been investigated [[110]]. MMP-2-deficient mice show severe arthritis,
arthritis 12352 arthritis in MMP-2 or MMP-9-deficient mice has been investigated [[110]]. MMP-2-deficient mice show severe arthritis , whereas MMP-9-deficient mice exhibit mild arthritis. These findings suggest a suppressive role for
arthritis 12405 investigated [[110]]. MMP-2-deficient mice show severe arthritis, whereas MMP-9-deficient mice exhibit mild arthritis . These findings suggest a suppressive role for MMP-2 and a pivotal role of MMP-9 in arthritis. MMP-3-deficient
arthritis 12499 mild arthritis. These findings suggest a suppressive role for MMP-2 and a pivotal role of MMP-9 in arthritis . MMP-3-deficient mice develop arthritis in a CIA model [[111]], and disruption of MMP-3 gene does not
arthritis 12539 a suppressive role for MMP-2 and a pivotal role of MMP-9 in arthritis. MMP-3-deficient mice develop arthritis in a CIA model [[111]], and disruption of MMP-3 gene does not prevent cartilage destruction.Over the
arthritis 13456 [[114],[115]]. It was expected to be a promising agent for RA therapy given results of animal models of arthritis [[116],[117]]. However, the compound did not prevent progression of joint destruction in RA patients
rheumatoid arthritis 2889 matrix metalloproteinases (MMPs), which are involved in the pathogenesis of numerous diseases, such as rheumatoid arthritis (RA).The mechanisms regulating MMP transcription have been clarified. Pro-inflammatory cytokines, including

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