Open Rheumatology Journal最新文献

{"title":"Profiling of hla-B alleles for association studies with ankylosing spondylitis in the chinese population.","authors":"Lin Yi,&nbsp;Jiucun Wang,&nbsp;Xinjian Guo,&nbsp;Maribel G Espitia,&nbsp;Enuo Chen,&nbsp;Shervin Assassi,&nbsp;Li Jin,&nbsp;Hejian Zou,&nbsp;John D Reveille,&nbsp;Xiaodong Zhou","doi":"10.2174/1874312920130628001","DOIUrl":"https://doi.org/10.2174/1874312920130628001","url":null,"abstract":"<p><p>Human leucocyte antigen (HLA) B*27 is a susceptibility allele to ankylosing spondylitis (AS). However, major AS-associated subtypes of HLA-B*27 and other HLA-B alleles vary in different ethnic populations. Herein, we examined HLA-B alleles in a total of 360 AS patients and 350 controls of Chinese Han ancestry. The HLA-B genotyping was performed with sequence-based typing (SBT) method. Six HLA-B*27 subtypes B*27:04, B*27:05, B*27:07, B*27:08, B*27:10 and B*27:15 were observed in the cohorts. HLA-B*27:04:01 and -B*27:05:02 appeared significantly increased in AS patients, which indicated as two major susceptibility alleles to AS. Homozygous B*27 was observed only in AS patients. There are 30 HLA-B alleles identified in the studies. HLA-B*15, especially B*15:01:01:01, appeared as the major allele type in the Chinese controls. Some common HLA-B alleles such as HLA-B*15, B*13, B*46 and B*51 were significantly reduced in Chinese AS patients. In conclusion, the studies profiled the HLA-B alleles, and identified major susceptibility subtypes of B27 to AS in Han Chinese population. </p>","PeriodicalId":39124,"journal":{"name":"Open Rheumatology Journal","volume":"7 ","pages":"51-4"},"PeriodicalIF":0.0,"publicationDate":"2013-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/48/71/TORJ-7-51.PMC3778539.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31757149","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Efficacy of Continuous Versus Intermittent Celecoxib Treatment in Osteoarthritis Patients with Body Mass Index ≥30 and <30 kg/m(2.).","authors":"George H Sands,&nbsp;Pritha Bhadra Brown,&nbsp;Margaret Noyes Essex","doi":"10.2174/1874312901307010032","DOIUrl":"https://doi.org/10.2174/1874312901307010032","url":null,"abstract":"<p><strong>Objective: </strong>Characterize the effect of body mass index (BMI) on the efficacy of continuous daily celecoxib treatment compared with intermittent celecoxib treatment.</p><p><strong>Methods: </strong>Prespecified exploratory analysis of a 24-week, double-blind, parallel-group, randomized, multicenter international study. 858 patients with knee or hip osteoarthritis (OA) were randomized to receive celecoxib 200 mg daily either as continuous or intermittent treatment. Efficacy was measured by Western Ontario and McMaster Universities Arthritis Index (WOMAC) total and subscale scores and the number of flare events.</p><p><strong>Results: </strong>Least squares mean increases (worsening) in WOMAC total scores were significantly less in the continuous treatment group than in the intermittent treatment group in patients with a BMI <30 kg/m(2) (1.33 vs 4.85; p=0.016) and in patients with a BMI ≥30 kg/m(2) (1.84 vs 5.12; p=0.019). There was a greater worsening in patients with a BMI ≥30 kg/m(2) than in those with a BMI <30 kg/m(2) in both the continuous and intermittent groups. Fewer flares were reported in the continuous treatment group than in the intermittent group in patients with a BMI <30 kg/m(2) (0.55 vs 0.88; p<0.0001) and ≥30 kg/m(2) (0.54 vs 0.97; p<0.0001). There were no differences in adverse events in the two BMI groups.</p><p><strong>Conclusions: </strong>Continuous celecoxib treatment was significantly more efficacious than intermittent use in patients with a BMI <30 kg/m(2) compared with obese patients (≥30 kg/m(2)) as assessed by WOMAC total scores and the number of flares. These data suggest that including weight loss as part of a treatment regimen for obese OA patients could be important.</p>","PeriodicalId":39124,"journal":{"name":"Open Rheumatology Journal","volume":"7 ","pages":"32-7"},"PeriodicalIF":0.0,"publicationDate":"2013-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d0/87/TORJ-7-32.PMC3731795.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31636567","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intra-articular hyaluronic Acid as treatment in elderly and middle-aged patients with knee osteoarthritis.","authors":"Demet Uçar,&nbsp;Demirhan Dıraçoğlu,&nbsp;Türker Süleyman,&nbsp;Nalan Capan","doi":"10.2174/1874312901307010038","DOIUrl":"https://doi.org/10.2174/1874312901307010038","url":null,"abstract":"<p><strong>Introduction: </strong>Osteoarthritis is the most common age-related degenerative joint disease. It affects all the joints containing hyaline cartilage. Knee osteoarthritis is the most cumbersome in terms of prevalence and disability. The aim of this study to evaluate the efficacy of intra-articular hyaluronic acid in patients with knee osteoarthritis with regard to joint pain and function, as well as patient satisfaction, assessed at one month and at one year, and by age group.</p><p><strong>Methods: </strong>In this prospective randomised study, 172 patients who were diagnosed knee OA and who received three consecutive intra-articular injections of HA weekly were included. Patients 65 years of age or older were accepted as the \"elderly group\", and those under 65 were accepted as the \"middle-aged group\". Clinical evaluations of efficacy and safety were conducted at the beginning of the study, one month after the third injection, and one year after the third injection.</p><p><strong>Results: </strong>In the two groups, the intragroup analysis revealed significant improvements following injection when compared with preinjection values. According to the last followup controls (after 12 months) in the middle-aged group, VAS activity pain, VAS rest pain, WOMAC physical function, and WOMAC pain values were found to be statistically lower when compared with pre-injection values. In the elderly group, no statistically significant differences were found between pre-injection and after 12 months.</p><p><strong>Conclusion: </strong>We can conclude that intra-articular joint HA injections are effective in both young and old patients with OA with regard to pain and functional status over a short-term period. Further, HA injections in patients younger than 65 years can be planned for a one-year period.</p>","PeriodicalId":39124,"journal":{"name":"Open Rheumatology Journal","volume":"7 ","pages":"38-41"},"PeriodicalIF":0.0,"publicationDate":"2013-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/d9/5e/TORJ-7-38.PMC3731797.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31636568","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory cells in tissues of gout patients and their correlations with comorbidities.","authors":"Syeling Lai,&nbsp;Xiaodong Zhou","doi":"10.2174/1874312901307010026","DOIUrl":"https://doi.org/10.2174/1874312901307010026","url":null,"abstract":"<p><strong>Background: </strong>The major pathological finding of gout is the deposition of monosodium urate monohydrate (MSU) crystals with inflammatory infiltrate in the tissue. There have been many reports of in vitro analysis of inflammatory mechanism and comorbidities in gout. However, the associations of immune response cells and comorbidities of gout have not been well documented. Our studies aimed to examine the immune cell types and quantity in gout tissues, and to define the association of individual cell type with comorbidities.</p><p><strong>Methods: </strong>Surgically resected or biopsied tissues from 48 patients diagnosed as gout were used for this study. Cell count was performed on Hemotoxylin and Eosin stained sections for macrophages, plasma cells, neutrophils and on immunostained slides for T and B lymphocytes.</p><p><strong>Results: </strong>Hyperlipidemia, hypertension and diabetes mellitus were seen in 70.8%, 87.5% and 37.5% of patients, respectively. There were 35.6% and 37.8% of patients who admitted history of smoking and alcohol intake, respectively. Mean serum uric acid level was 8.5 mg/dl. The average body mass index was 30.1 kg/m(2). H&E stained tissue sections demonstrated the crystalline deposits rimmed by palisading multinucleated giant cells, macrophages, neutrophils, plasma cells, T and B cells. Significant correlations between the clinical features and tissue inflammatory cells were observed in hyperlipidemia with number of T cells (p = 0.0363), hypertension with number of T cells and B cells (p = 0.0138 and 0.0033, respectively), diabetes mellitus with macrophages (p = 0.0016), and uric acid level with giant cells (p = 0.0088).</p><p><strong>Conclusion: </strong>Comorbidity factors including hyperlipidemia, hypertension and diabetes are significantly associated with the inflammatory cells in the tissues.</p>","PeriodicalId":39124,"journal":{"name":"Open Rheumatology Journal","volume":"7 ","pages":"26-31"},"PeriodicalIF":0.0,"publicationDate":"2013-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8d/31/TORJ-7-26.PMC3681035.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31628406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MEFV Variants in Patients with PFAPA Syndrome in Japan.","authors":"Shoichiro Taniuchi,&nbsp;Ryuta Nishikomori,&nbsp;Anna Iharada,&nbsp;Shoji Tuji,&nbsp;Toshio Heike,&nbsp;Kazunari Kaneko","doi":"10.2174/1874312901307010022","DOIUrl":"https://doi.org/10.2174/1874312901307010022","url":null,"abstract":"<p><strong>Background: </strong>The pathogenesis of PFAPA (periodic fever, aphthous stomatitis, pharyngitis, adenitis) syndrome is unknown as yet. In order to understand whether genes implicated in other auto-inflammatory diseases might be involved in the pathogenesis of PFAPA, all variants in the genes causing familial Mediterranean fever (FMF), tumor necrosis factor (TNF) receptor-associated periodic syndrome (TRAPS), and Hyper IgD syndrome were analyzed in children with PFAPA.</p><p><strong>Patients and methods: </strong>All variants in MEFV, TNFRSF1A, and MVK were analyzed in 20 patients with PFAPA. PFAPA were diagnosed by previous published criteria. The findings of all analyses in PFAPA patients were compared with those of unaffected normal subjects (n=62).</p><p><strong>Results: </strong>In the 13 children of 20 with PFAPA, the heterozygous variants of MEFV (5 patients: E148Q-L110P, 2 patients: E148Q, 1 patient: E148Q-L110P/E148Q, 1 patient: E148Q-P369S-R408Q-E84K, 1 patient: E148Q-L110P-P369S-A408G, 1 patient: R202Q, 1 patient: P115R) were found. No variants belonging to TNFRSF1A or MVK were detected in children with PFAPA. The frequency of the E148Q-L110P variants in children with PFAPA was significantly higher than that observed in unaffected normal subjects (7/20 versus 8/62). The duration of the episodes of illness in PFAPA children with MEFV variants was shorter than that of patients without variants.</p><p><strong>Conclusion: </strong>Genes involved in the development and progression of MEFV may affect the incidence and the phenotype of PFAPA in children.</p>","PeriodicalId":39124,"journal":{"name":"Open Rheumatology Journal","volume":"7 ","pages":"22-5"},"PeriodicalIF":0.0,"publicationDate":"2013-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/24/f8/TORJ-7-22.PMC3681033.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31216622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human Endogenous Retroviruses (HERVs) and Autoimmune Rheumatic Disease: Is There a Link?","authors":"Nicola Tugnet,&nbsp;Paul Rylance,&nbsp;Denise Roden,&nbsp;Malgorzata Trela,&nbsp;Paul Nelson","doi":"10.2174/1874312901307010013","DOIUrl":"https://doi.org/10.2174/1874312901307010013","url":null,"abstract":"<p><p>Autoimmune rheumatic diseases, such as RA and SLE, are caused by genetic, hormonal and environmental factors. Human Endogenous Retroviruses (HERVs) may be triggers of autoimmune rheumatic disease. HERVs are fossil viruses that began to be integrated into the human genome some 30-40 million years ago and now make up 8% of the genome. Evidence suggests HERVs may cause RA and SLE, among other rheumatic diseases. The key mechanisms by which HERVS are postulated to cause disease include molecular mimicry and immune dysregulation. Identification of HERVs in RA and SLE could lead to novel treatments for these chronic conditions. This review summarises the evidence for HERVs as contributors to autoimmune rheumatic disease and the clinical implications and mechanisms of pathogenesis are discussed.</p>","PeriodicalId":39124,"journal":{"name":"Open Rheumatology Journal","volume":"7 ","pages":"13-21"},"PeriodicalIF":0.0,"publicationDate":"2013-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/1b/d4/TORJ-7-13.PMC3636489.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31492811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cost-effectiveness modelling of sequential biologic strategies for the treatment of moderate to severe rheumatoid arthritis in Finland.","authors":"K Puolakka,&nbsp;H Blåfield,&nbsp;M Kauppi,&nbsp;R Luosujärvi,&nbsp;R Peltomaa,&nbsp;T Leikola-Pelho,&nbsp;K Sennfalt,&nbsp;A Beresniak","doi":"10.2174/1874312901206010038","DOIUrl":"https://doi.org/10.2174/1874312901206010038","url":null,"abstract":"<p><strong>Objective: </strong>The main objective was to compare the cost-effectiveness of therapeutic options in moderate or severe rheumatoid arthritis (RA) when a clinical response to a first TNF-blocker, either etanercept (ETA), adalimumab (ADA), or infliximab (INF), is insufficient.</p><p><strong>Methods: </strong>Effectiveness criteria were defined as remission (RS), low disease activity (LDAS), and moderate to high disease activity (MHDAS). Cost-effectiveness was derived as cost per day in RS and in LDAS using simulation modelling to assess six sequential biologic strategies over 2 years. Each sequential treatment strategy was composed of three biologic agents and included a first anti-TNF agent, ETA, ADA or INF, followed by either abatacept (ABA) or rituximab (RTX) as a second therapeutic option in case of an insufficient response, followed by another anti-TNF agent in case of further insufficient response.</p><p><strong>Results: </strong>Over two years and taking into account biologic costs, the following estimated mean costs per day in RS and LDAS were respectively of €829 and €428 for the biologic sequence composed of ADA-ABA-ETA, €1292 and €516 for the sequence ADA-RTX-ETA, €829 and €429 for the sequence ETA-ABA-ADA, €1292 and €517 for the sequence ETARTX- ADA, €840 and €434 for the sequence INF-ABA-ETA, and €1309 and €523 for the sequence INF-RTX-ETA.</p><p><strong>Conclusion: </strong>The treatment sequences including ABA as the second biologic option appear more cost-effective than those including RTX in a patients with moderate to severe RA and an insufficient response to a first anti-TNF agent.</p>","PeriodicalId":39124,"journal":{"name":"Open Rheumatology Journal","volume":"6 ","pages":"38-43"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/bc/1a/TORJ-6-38.PMC3349947.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30615653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of etoricoxib, celecoxib, lumiracoxib, non-selective NSAIDs, and acetaminophen in osteoarthritis: a mixed treatment comparison.","authors":"Wb Stam,&nbsp;Jp Jansen,&nbsp;Sd Taylor","doi":"10.2174/1874312901206010006","DOIUrl":"https://doi.org/10.2174/1874312901206010006","url":null,"abstract":"<p><strong>Objective: </strong>To compare the efficacy of etoricoxib, lumiracoxib, celecoxib, non-selective (ns) NSAIDs and acetaminophen in the treatment of osteoarthritis (OA) METHODS: Randomized placebo controlled trials investigating the effects of acetaminophen 4000mg, diclofenac 150mg, naproxen 1000mg, ibuprofen 2400mg, celecoxib 100-400mg, lumiracoxib 100-400mg, and etoricoxib 30-60mg with treatment duration of at least two weeks were identified with a systematic literature search. The endpoints of interest were pain, physical function and patient global assessment of disease status (PGADS). Pain and physical function reported on different scales (VAS or LIKERT) were translated into effect sizes (ES). An ES 0.2 - 0.5 was defined as a \"small\" treatment effect, whereas ES of 0.5 - 0.8 and > 0.8 were defined as \"moderate\" and \"large\", respectively. A negative effect indicated superior effects of the treatment group compared to the control group. Results of all trials were analyzed simultaneously with a Bayesian mixed treatment comparison.</p><p><strong>Results: </strong>There is a >95% probability that etoricoxib (30 or 60mg) shows the greatest improvement in pain and physical function of all interventions compared. ESs of etoricoxib 30mg relative to placebo, celecoxib 200mg, ibuprofen 2400mg, and diclofenac 150mg were -0.66 (95% Credible Interval -0.83; -0.49), -0.32 (-0.50; -0.14), -0.25 (-0.53; 0.03), and -0.17 (-0.41; 0.08), respectively. Regarding physical functioning, ESs of etoricoxib 30mg relative to placebo, celecoxib 200mg, ibuprofen 2400mg, and diclofenac 150mg were -0.61 (-0.76; -0.46), -0.27 (-0.43; -0.10), -0.20 (-0.47; 0.07), and -0.09 (- 0.33; 0.14) respectively. The greatest improvements in PGADS were expected with either etoricoxib or diclofenac.</p><p><strong>Conclusion: </strong>The current study estimated the efficacy of acetaminophen, nsNSAIDs, and COX-2 selective NSAIDs in OA and found that etoricoxib 30 mg is likely to result in the greatest improvements in pain and physical function. Differences in PGADS between interventions were smaller.</p>","PeriodicalId":39124,"journal":{"name":"Open Rheumatology Journal","volume":"6 ","pages":"6-20"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2174/1874312901206010006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30615652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of the NLRP3 Inflammasome in Fibrosis.","authors":"Carol M Artlett","doi":"10.2174/1874312901206010080","DOIUrl":"https://doi.org/10.2174/1874312901206010080","url":null,"abstract":"<p><p>Fibrosis leads to the deposition of collagens in organs and tissues. The resulting pathology induces a loss of function in the organ it is manifested in and this loss of function modulates the morbidity and mortality in that individual. Indeed, approximately 45% of all deaths in the Western world can be attributed to fibrosis and there are no FDA approved drugs for the treatment of fibrosis. The recent discovery of the inflammasome has led to a plethora of studies investigating this inflammatory signaling pathway in a wide variety of pathogen associated diseases. Many studies have focused on the NLRP3 inflammasome and this inflammasome is activated by a wide variety of cellular alarm signals. Once activated, caspase-1 is cleaved, inducing the secretion of IL-1β and IL-18 that signal to aid in the clearance of invading organisms. However, as the knowledge of the inflammasome has expanded, it was found that it can directly control collagen synthesis, leading to the increased deposition of collagens in the tissues such as the lung, liver, heart, and skin. Mice lacking the inflammasome adaptor protein, ASC, failed to become fibrotic when exposed to bleomycin. Inhibition of caspase-1 activity in fibroblasts from patients with the fibrotic disease systemic sclerosis, decreased collagen synthesis and reduced α-smooth muscle actin expression in myofibroblasts. Taken together, these observations suggest that the inflammasome can drive the fibrotic response and paves the way for novel therapeutics to be identified.</p>","PeriodicalId":39124,"journal":{"name":"Open Rheumatology Journal","volume":"6 ","pages":"80-6"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/8b/c0/TORJ-6-80.PMC3395884.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30767124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mediators of fibrosis.","authors":"Maria Trojanowska","doi":"10.2174/1874312901206010070","DOIUrl":"https://doi.org/10.2174/1874312901206010070","url":null,"abstract":"Progressive, uncontrolled deposition of extracellular matrix proteins leading to scar tissue formation and organ failure represents a final common pathway of tissue response to chronic injury. The nature of the insult varies between organs and tissues and may include viral infections or toxic agents, but in most cases the specific trigger remains unknown. Extensive research on the mechanisms of fibrosis has greatly contributed to a better understanding of the pathological mechanisms involved in this process. While we are learning more about the pathways that contribute to fibrosis, it would be important to integrate this new information with the large body of existing knowledge on the profibrotic mediators, especially Transforming Growth factor (TGF ). TGF is one of the most potent inducers of extracellular matrix and has long been considered to be a principal mediator of fibrosis. In addition to activation of both Smad-dependent and Smad-independent signaling pathways, TGF is involved in an extensive crosstalk with multiple other cellular pathways. Better understanding of the regulatory networks governing the fibrotic response at the cellular level will help to define the key regulatory molecules and advance the design of logical therapeutic targets. This series of articles will highlight some of the new developments in the field of fibrotic mediators.","PeriodicalId":39124,"journal":{"name":"Open Rheumatology Journal","volume":"6 ","pages":"70-1"},"PeriodicalIF":0.0,"publicationDate":"2012-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/17/d9/TORJ-6-70.PMC3395879.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30767122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}