TY - JOUR
T1 - Metabolic Checkpoints in Rheumatoid Arthritis
AU - Pucino, Valentina
AU - Certo, Michelangelo
AU - Varricchi, Gilda
AU - Marone, Giancarlo
AU - Ursini, Francesco
AU - Rossi, Francesca Wanda
AU - De Paulis, Amato
AU - Mauro, Claudio
AU - Raza, Karim
AU - Buckley, Christopher Dominic
N1 - Copyright © 2020 Pucino, Certo, Varricchi, Marone, Ursini, Rossi, De Paulis, Mauro, Raza and Buckley.
PY - 2020
Y1 - 2020
N2 - 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.
AB - 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.
KW - immunity
KW - immunometabolism
KW - mediators of inflammation
KW - metabolism
KW - rheumatoid arthritis
U2 - 10.3389/fphys.2020.00347
DO - 10.3389/fphys.2020.00347
M3 - Review article
C2 - 32362840
VL - 11
SP - 1
EP - 12
JO - Frontiers in Physiology
JF - Frontiers in Physiology
SN - 1664-042X
ER -