Abstract
Adipokines are adipose tissue-derived factors not only playing an important role in metabolism but also influencing other central processes of the body, such as inflammation. In autoimmune diseases, adipokines are involved in inflammatory pathways affecting different cell types. Many rheumatic diseases belong to the group of autoimmune diseases, for example rheumatoid arthritis (RA) and psoriatic arthritis. Due to the autoimmune responses, a chronic inflammatory milieu develops, which affects the whole body, including adipose tissue. Metabolic alterations such as obesity influence inflammatory responses in autoimmune diseases. Adipokines are bioactive mediators mainly produced by adipose tissue. Due to alterations of systemic adipokine levels, their role as biomarkers with diagnostic potential has been suggested in the context of rheumatic diseases. In the affected joints of RA patients, different synoviocytes but also osteoclasts, osteoblasts, and chondrocytes produce several adipokines, contributing to the unique inflammatory microenvironment. Adipokines have been shown to be potent modulatory effectors on different cell types of the immune system but also local cells in synovial tissue, cartilage, and bone. This review highlights the most recent findings on the role of adipokines in the pathophysiology of inflammatory arthritis with a distinct focus on RA in the quickly developing research field.
Highlights
Disorders affecting the joint can be divided in two central groups
It was shown in this study that the levels of vaspin and neutrophil gelatinase-associated lipocalin as well as the apolipoprotein B1/A1 ratios were significantly higher in psoriatic arthritis (PsA) compared to controls, but none of the factors were correlated with disease activity [83]
It was shown that metabolic factors, factors produced in high amounts by adipose tissue and adipocytes, contribute to inflammatory processes in rheumatoid arthritis (RA) and in many other autoimmune diseases
Summary
Disorders affecting the joint can be divided in two central groups. Primary inflammatory autoimmune arthritides consist of rheumatoid arthritis (RA) and spondyloarthritides, including psoriatic arthritis (PsA) and ankylosing spondylitis. Though cartilage degradation is a central feature of OA, resulting in an inflammatory response due to mechanical joint damage, the whole joint is affected, including adjacent bone, which involves the formation of osteophytes [1]. RA is an autoimmune disorder characterized by severe chronic inflammation early within the disease, leading to irreversible joint damage if left untreated [2]. PsA and RA are both rheumatic chronic inflammatory diseases sharing similarities such as synovitis and differences in the pathophysiology This includes a different vascular pattern in the affected joints [6], a less pronounced synovial hyperplasia in PsA compared to RA patients [7], and the cell infiltrates at the inflamed synovial–entheseal complex being more prominent in PsA patients [8]. Due to alterations of tissues or tissue components in the course of the disease as well as due to autoimmune responses, the organism is no longer able to terminate the pathophysiological inflammatory circle, resulting in continuous tissue damage and, loss of function and quality-of-life impairment
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