Review: Synovial cell mtabolism and chronic inflammation in rheumatoid arthritis
Metabolomic studies of body fluids show that immune‐mediated inflammatory diseases such as rheumatoid arthritis (RA) are associated with metabolic disruption. This is likely to reflect the increased bioenergetic and biosynthetic demands of sustained inflammation and changes in nutrient and oxygen av...
| Main Authors: | , , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
Wiley
2018
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| _version_ | 1797067697075257344 |
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| author | Falconer, J Murphy, A Young, S Clark, A Tiziani, S Guma, M Buckley, C |
| author_facet | Falconer, J Murphy, A Young, S Clark, A Tiziani, S Guma, M Buckley, C |
| author_sort | Falconer, J |
| collection | OXFORD |
| description | Metabolomic studies of body fluids show that immune‐mediated inflammatory diseases such as rheumatoid arthritis (RA) are associated with metabolic disruption. This is likely to reflect the increased bioenergetic and biosynthetic demands of sustained inflammation and changes in nutrient and oxygen availability in damaged tissue. The synovial membrane lining layer is the principal site of inflammation in RA. Here, the resident cells are fibroblast‐like synoviocytes (FLS) and synovial tissue macrophages, which are transformed toward overproduction of enzymes that degrade cartilage and bone and cytokines that promote immune cell infiltration. Recent studies have shown metabolic changes in both FLS and macrophages from RA patients, and these may be therapeutically targetable. However, because the origins and subset‐specific functions of synoviocytes are poorly understood, and the signaling modules that control metabolic deviation in RA synovial cells are yet to be explored, significant additional research is needed to translate these findings to clinical application. Furthermore, in many inflamed tissues, different cell types can forge metabolic collaborations through solute carriers in their membranes to meet a high demand for energy or biomolecules. Such relationships are likely to exist in the synovium and have not been studied. Finally, it is not yet known whether metabolic change is a consequence of disease or whether primary changes to cellular metabolism might underlie or contribute to the pathogenesis of early‐stage disease. In this review article, we collate what is known about metabolism in synovial tissue cells and highlight future directions of research in this area. |
| first_indexed | 2024-03-06T22:00:00Z |
| format | Journal article |
| id | oxford-uuid:4e425bb2-c4e5-426c-86ba-42d2a89a9285 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T22:00:00Z |
| publishDate | 2018 |
| publisher | Wiley |
| record_format | dspace |
| spelling | oxford-uuid:4e425bb2-c4e5-426c-86ba-42d2a89a92852022-03-26T16:00:10ZReview: Synovial cell mtabolism and chronic inflammation in rheumatoid arthritisJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:4e425bb2-c4e5-426c-86ba-42d2a89a9285EnglishSymplectic Elements at OxfordWiley2018Falconer, JMurphy, AYoung, SClark, ATiziani, SGuma, MBuckley, CMetabolomic studies of body fluids show that immune‐mediated inflammatory diseases such as rheumatoid arthritis (RA) are associated with metabolic disruption. This is likely to reflect the increased bioenergetic and biosynthetic demands of sustained inflammation and changes in nutrient and oxygen availability in damaged tissue. The synovial membrane lining layer is the principal site of inflammation in RA. Here, the resident cells are fibroblast‐like synoviocytes (FLS) and synovial tissue macrophages, which are transformed toward overproduction of enzymes that degrade cartilage and bone and cytokines that promote immune cell infiltration. Recent studies have shown metabolic changes in both FLS and macrophages from RA patients, and these may be therapeutically targetable. However, because the origins and subset‐specific functions of synoviocytes are poorly understood, and the signaling modules that control metabolic deviation in RA synovial cells are yet to be explored, significant additional research is needed to translate these findings to clinical application. Furthermore, in many inflamed tissues, different cell types can forge metabolic collaborations through solute carriers in their membranes to meet a high demand for energy or biomolecules. Such relationships are likely to exist in the synovium and have not been studied. Finally, it is not yet known whether metabolic change is a consequence of disease or whether primary changes to cellular metabolism might underlie or contribute to the pathogenesis of early‐stage disease. In this review article, we collate what is known about metabolism in synovial tissue cells and highlight future directions of research in this area. |
| spellingShingle | Falconer, J Murphy, A Young, S Clark, A Tiziani, S Guma, M Buckley, C Review: Synovial cell mtabolism and chronic inflammation in rheumatoid arthritis |
| title | Review: Synovial cell mtabolism and chronic inflammation in rheumatoid arthritis |
| title_full | Review: Synovial cell mtabolism and chronic inflammation in rheumatoid arthritis |
| title_fullStr | Review: Synovial cell mtabolism and chronic inflammation in rheumatoid arthritis |
| title_full_unstemmed | Review: Synovial cell mtabolism and chronic inflammation in rheumatoid arthritis |
| title_short | Review: Synovial cell mtabolism and chronic inflammation in rheumatoid arthritis |
| title_sort | review synovial cell mtabolism and chronic inflammation in rheumatoid arthritis |
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