Review: Synovial Cell Metabolism and Chronic Inflammation in Rheumatoid Arthritis

Arthritis and Rheumatology - Tập 70 Số 7 - Trang 984-999 - 2018
Jane Falconer1, Anne N. Murphy2, Stephen P. Young2, Andrew R. Clark3, Stefano Tiziani4, Mònica Gumà2,5, Christopher D. Buckley6,7
1University of Birmingham Queen Elizabeth Hospital and National Institute for Health Research Birmingham Biomedical Research Centre Birmingham UK
2Rheumatology Research Group, Institute of Inflammation and Ageing, College of Medical and Dental Sciences, University of Birmingham, Queen Elizabeth Hospital, Birmingham, UK
3University of Birmingham, Queen Elizabeth Hospital, Birmingham, UK
4University of Texas at Austin
5The Kennedy Institute of Rheumatology, University of Oxford, Oxford, UK
6University of Birmingham Queen Elizabeth Hospital National Institute for Health Research Birmingham Biomedical Research Centre Birmingham UK
7University Of Oxford, Oxford, UK

Tóm tắt

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.

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Arthritis and Rheumatology

Tập 70 Số 7

984-999

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