| Summary: | 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, adipocytokines 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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