FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4386757514> ?p ?o ?g. }

• W4386757514 endingPage "8" @default.
• W4386757514 startingPage "1" @default.
• W4386757514 abstract "ABSTRACTIntroduction Rheumatoid arthritis is a chronic inflammatory disease marked by systemic symptoms and joint degeneration. Interestingly, the development and progression of rheumatoid arthritis have been linked to the microbiome, notably the gut microbiome. Dysbiosis, an alteration in the gut microbiome, has been connected to the etiology and pathogenesis of rheumatoid arthritis. For instance, dysbiosis increases intestinal permeability and promotes the movement of bacteria and its products, which in turn triggers and aggravates systemic inflammation.Areas covered The correlation between the gut microbiome and RA. Triggers of RA including dysbiosis. The therapeutic potential of the gut microbiome in RA due to its critical function in influencing the immune response. The fecal microbiota transplantation (FMT), a therapeutic strategy that involves the transfer of healthy fecal microbiota from a donor to a recipient, has produced encouraging results in the treatment of several autoimmune illnesses, including rheumatoid arthritis.Expert opinion The role of the gut microbiome in RA is critical, and serves as a basis for the etiology, pathogenesis, as well as having therapeutic implications. In our opinion, FMT is an excellent example for this correlation. Still, more investigations and well-designed studied are needed in order to make firm conclusions and recommendations.KEYWORDS: Autoimmunityfecal microbial transplantationgut microbiomemicrobiome, rheumatoid arthritisDisclaimerAs a service to authors and researchers we are providing this version of an accepted manuscript (AM). Copyediting, typesetting, and review of the resulting proofs will be undertaken on this manuscript before final publication of the Version of Record (VoR). During production and pre-press, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal relate to these versions also. Declaration of interestThe authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.AcknowledgmentsThe authors would like to thank Abdulkarim Alwani (Istanbul Medipol University) for providing the Figure design.Reviewer disclosuresPeer reviewers on this manuscript have no relevant financial or other relationships to disclose.Article highlightsThe etiology and pathogenesis of rheumatoid arthritis is still under active research.The gut microbiome has been investigated in the last decades as a key element in the pathogenesis of rheumatoid arthritis.Alterations in gut microbiome, the “dysbiosis”, were shown to take place early in the disease.Figuring out and understanding the role of gut microbiome in rheumatoid arthritis have significant implications in the treatment of the disease.Fecal microbiota transplantation has shown beneficial effects in animal models as well as patients with rheumatoid arthritis.Figure 1: Factors influencing the onset of rheumatoid arthritis (RA). The development of RA is influenced by both environmental (smoking, obesity, infections with specific pathogens like Porphyromonas gingivialis), as well as genetic (epigenetic alterations, genetic polymorphisms influencing antigen presentation, such as the HLA genes HLA-DRB1*01/04), T- and B cell function, cytokine production, and signal transduction after immune cell activation). More recently, alterations in oral and gut microbiota bacterial compositions also induce arthritis. Additionally, synovial damage and synovial fibroblast hyperplasia can contribute to the development of RA by inducing inflammatory conditions. Overall, these mechanisms lead to changes in autoantigens (mostly through citrullination), which results in neoepitopes by losing their surface charge and becoming more susceptible to proteolytic destruction.Display full sizeAdditional informationFundingThis paper was not funded." @default.
• W4386757514 created "2023-09-16" @default.
• W4386757514 creator A5010387739 @default.
• W4386757514 creator A5074738902 @default.
• W4386757514 creator A5089544748 @default.
• W4386757514 date "2023-09-15" @default.
• W4386757514 modified "2023-09-28" @default.
• W4386757514 title "Triggers and regulation: the gut microbiome in rheumatoid arthritis" @default.
• W4386757514 cites W108172154 @default.
• W4386757514 cites W1775279835 @default.
• W4386757514 cites W1943338444 @default.
• W4386757514 cites W1970971642 @default.
• W4386757514 cites W1972505691 @default.
• W4386757514 cites W1975908075 @default.
• W4386757514 cites W1976068756 @default.
• W4386757514 cites W1986722574 @default.
• W4386757514 cites W2012606594 @default.
• W4386757514 cites W2015246717 @default.
• W4386757514 cites W2016947725 @default.
• W4386757514 cites W2034066083 @default.
• W4386757514 cites W2034277871 @default.
• W4386757514 cites W2048698197 @default.
• W4386757514 cites W2055552847 @default.
• W4386757514 cites W2080836926 @default.
• W4386757514 cites W2085175109 @default.
• W4386757514 cites W2108355568 @default.
• W4386757514 cites W2110826367 @default.
• W4386757514 cites W2112033983 @default.
• W4386757514 cites W2113368377 @default.
• W4386757514 cites W2113552312 @default.
• W4386757514 cites W2123027776 @default.
• W4386757514 cites W2126046570 @default.
• W4386757514 cites W2129114020 @default.
• W4386757514 cites W2133607388 @default.
• W4386757514 cites W2150780552 @default.
• W4386757514 cites W2156904705 @default.
• W4386757514 cites W2159560463 @default.
• W4386757514 cites W2167927725 @default.
• W4386757514 cites W2169364567 @default.
• W4386757514 cites W2281990250 @default.
• W4386757514 cites W2336588424 @default.
• W4386757514 cites W2336817596 @default.
• W4386757514 cites W2398619572 @default.
• W4386757514 cites W2479329805 @default.
• W4386757514 cites W2489043195 @default.
• W4386757514 cites W2511630240 @default.
• W4386757514 cites W2519199594 @default.
• W4386757514 cites W2522777940 @default.
• W4386757514 cites W2531009503 @default.
• W4386757514 cites W2587506066 @default.
• W4386757514 cites W2605545078 @default.
• W4386757514 cites W2610362303 @default.
• W4386757514 cites W2623617647 @default.
• W4386757514 cites W2626193283 @default.
• W4386757514 cites W2742690586 @default.
• W4386757514 cites W2767894846 @default.
• W4386757514 cites W2790669451 @default.
• W4386757514 cites W2802137035 @default.
• W4386757514 cites W2886363262 @default.
• W4386757514 cites W2896285785 @default.
• W4386757514 cites W2902525413 @default.
• W4386757514 cites W2910898181 @default.
• W4386757514 cites W2913429571 @default.
• W4386757514 cites W2946017293 @default.
• W4386757514 cites W2957585395 @default.
• W4386757514 cites W2981258342 @default.
• W4386757514 cites W2981593585 @default.
• W4386757514 cites W2983698537 @default.
• W4386757514 cites W3012542016 @default.
• W4386757514 cites W3014146563 @default.
• W4386757514 cites W3019025224 @default.
• W4386757514 cites W3024444425 @default.
• W4386757514 cites W3037169575 @default.
• W4386757514 cites W3084302616 @default.
• W4386757514 cites W3100739275 @default.
• W4386757514 cites W3102747965 @default.
• W4386757514 cites W3108788068 @default.
• W4386757514 cites W3114695099 @default.
• W4386757514 cites W3134475720 @default.
• W4386757514 cites W3174485034 @default.
• W4386757514 cites W3177146939 @default.
• W4386757514 cites W3203997343 @default.
• W4386757514 cites W3206785112 @default.
• W4386757514 cites W4205839480 @default.
• W4386757514 cites W4211111012 @default.
• W4386757514 cites W4213202281 @default.
• W4386757514 cites W4241917186 @default.
• W4386757514 cites W4281775795 @default.
• W4386757514 cites W4289927814 @default.
• W4386757514 cites W4290466233 @default.
• W4386757514 cites W4307155462 @default.
• W4386757514 cites W4313889061 @default.
• W4386757514 cites W4324332303 @default.
• W4386757514 doi "https://doi.org/10.1080/1744666x.2023.2260103" @default.
• W4386757514 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37712213" @default.
• W4386757514 hasPublicationYear "2023" @default.
• W4386757514 type Work @default.
• W4386757514 citedByCount "0" @default.

• next