AI Article Synopsis

  • Studies show that metabolism, immunity, and inflammation are interconnected, especially in rheumatoid arthritis (RA), as immune cells produce various signaling molecules that drive inflammation.
  • The synovial membrane is crucial to RA, exhibiting distinct metabolic behaviors that affect inflammation, prognosis, and treatment responses.
  • Ongoing research aims to clarify whether metabolic changes contribute to RA development or are effects of the disease, which could help identify new treatment strategies.

Article Abstract

Several studies have highlighted the interplay between metabolism, immunity and inflammation. Both tissue resident and infiltrating immune cells play a major role in the inflammatory process of rheumatoid arthritis (RA) via the production of cytokines, adipo-cytokines and metabolic intermediates. These functions are metabolically demanding and require the most efficient use of bioenergetic pathways. The synovial membrane is the primary site of inflammation in RA and exhibits distinctive histological patterns characterized by different metabolism, prognosis and response to treatment. In the RA synovium, the high energy demand by stromal and infiltrating immune cells, causes the accumulation of metabolites, and adipo-cytokines, which carry out signaling functions, as well as activating transcription factors which act as metabolic sensors. These events drive immune and joint-resident cells to acquire pro-inflammatory effector functions which in turn perpetuate chronic inflammation. Whether metabolic changes are a consequence of the disease or one of the causes of RA pathogenesis is still under investigation. This review covers our current knowledge of cell metabolism in RA. Understanding the intricate interactions between metabolic pathways and the inflammatory and immune responses will provide more awareness of the mechanisms underlying RA pathogenesis and will identify novel therapeutic options to treat this disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7180190PMC
http://dx.doi.org/10.3389/fphys.2020.00347DOI Listing

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