Location, location, location: how the tissue microenvironment affects inflammation in RA

Buckley, Christopher D.; Ospelt, Caroline; Midwood, Kim S.

doi:10.1038/s41584-020-00570-2

Cited by 92 publications

(82 citation statements)

References 183 publications

(163 reference statements)

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“…This spatiotemporally limited expression pattern is particularly prominent in the heart (reviewed in [ 12 , 13 ]). Accumulating evidence has shown diverse and important roles for TNC in responses to injury as well as cancer stroma [ 14 , 15 ], particularly in the regulation of inflammation [ 16 , 17 ]; however, neither the knockout nor overexpression of TNC induces a distinct phenotype during heart development [ 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Tenascin-C in Heart Diseases—The Role of Inflammation

Imanaka‐Yoshida

2021

IJMS

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Tenascin-C (TNC) is a large extracellular matrix (ECM) glycoprotein and an original member of the matricellular protein family. TNC is transiently expressed in the heart during embryonic development, but is rarely detected in normal adults; however, its expression is strongly up-regulated with inflammation. Although neither TNC-knockout nor -overexpressing mice show a distinct phenotype, disease models using genetically engineered mice combined with in vitro experiments have revealed multiple significant roles for TNC in responses to injury and myocardial repair, particularly in the regulation of inflammation. In most cases, TNC appears to deteriorate adverse ventricular remodeling by aggravating inflammation/fibrosis. Furthermore, accumulating clinical evidence has shown that high TNC levels predict adverse ventricular remodeling and a poor prognosis in patients with various heart diseases. Since the importance of inflammation has attracted attention in the pathophysiology of heart diseases, this review will focus on the roles of TNC in various types of inflammatory reactions, such as myocardial infarction, hypertensive fibrosis, myocarditis caused by viral infection or autoimmunity, and dilated cardiomyopathy. The utility of TNC as a biomarker for the stratification of myocardial disease conditions and the selection of appropriate therapies will also be discussed from a clinical viewpoint.

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Section: Introductionmentioning

confidence: 99%

Tenascin-C in Heart Diseases—The Role of Inflammation

Imanaka‐Yoshida

2021

IJMS

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“…These specialized synovial tissue niches undergo cellular remodeling in response to inflammation and contain specific subsets of fibroblasts. 27 The spatial and temporal heterogeneity of synovial fibroblasts underpins their pathogenic role in inflammatory joint disease. 47 Fibroblast heterogeneity is driven by anatomical location in the tissue, 100 microenvironmental instructive signals, 62 and interaction with tissue-resident leukocytes.…”

Section: Con Cluding Remark Smentioning

confidence: 99%

“…Lining layer fibroblasts directly contribute to the composition of the synovial fluid by producing lubricin (proteoglycan 4) and hyaluronic acid that lubricate the joint during locomotion 20 . These cells also regulate ion transport and deposit extracellular matrix made up of type III, IV, V, and VI collagen and laminin allowing nutrient exchange between the synovial fluid and the synovial membrane 27 …”

Section: Synovial Fibroblasts In the Healthy Jointmentioning

confidence: 99%

“…The formation of pannus tissue, a well‐described architectural feature of the chronically inflamed joint, 25 is comprised of hypertrophic synovium, composed of macrophages and fibroblasts that produce destructive enzymes that degrade articular cartilage and bone 26 . The cellular components and mechanisms underlying the disease‐specific remodeling of the synovium have yet to be fully elucidated 27 …”

Section: Introductionmentioning

confidence: 99%

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Fibroblast pathology in inflammatory joint disease

Marsh

Kemble

Nisa

et al. 2021

Immunological Reviews

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In this review, we highlight new approaches and applications of single-cell profiling techniques 1,2 and how these data are leading to unique insights into the phenotypic and functional heterogeneity of fibroblasts in the joint. 3 Finally, we will discuss how defining this previously underappreciated fibroblast heterogeneity in rheumatoid arthritis (RA) is leading to the identification of pathological fibroblast cell states that could be therapeutically targeted in inflammatory joint disease. 4 | Rheumatoid arthritisRA is a prototypic immune-mediated inflammatory disease characterized by persistent synovial joint inflammation that, if untreated, leads to progressive joint damage. [5][6][7] While the

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“…Fibroblasts build lining layers surrounding the joint cavitation. Local destruction of this physiological barrier primes inflammatory processes [ 28 ]. Therefore, tissue-specific insights in IMIDs are of interest in order to select the one with the highest chance of success from the available therapeutics.…”

Section: Spatial Sequencingmentioning

confidence: 99%

The Potential of OMICs Technologies for the Treatment of Immune-Mediated Inflammatory Diseases

Anchang

Raimondo

et al. 2021

IJMS

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Immune-mediated inflammatory diseases (IMIDs), such as inflammatory bowel diseases and inflammatory arthritis (e.g., rheumatoid arthritis, psoriatic arthritis), are marked by increasing worldwide incidence rates. Apart from irreversible damage of the affected tissue, the systemic nature of these diseases heightens the incidence of cardiovascular insults and colitis-associated neoplasia. Only 40–60% of patients respond to currently used standard-of-care immunotherapies. In addition to this limited long-term effectiveness, all current therapies have to be given on a lifelong basis as they are unable to specifically reprogram the inflammatory process and thus achieve a true cure of the disease. On the other hand, the development of various OMICs technologies is considered as “the great hope” for improving the treatment of IMIDs. This review sheds light on the progressive development and the numerous approaches from basic science that gradually lead to the transfer from “bench to bedside” and the implementation into general patient care procedures.

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Location, location, location: how the tissue microenvironment affects inflammation in RA

Cited by 92 publications

References 183 publications

Tenascin-C in Heart Diseases—The Role of Inflammation

Tenascin-C in Heart Diseases—The Role of Inflammation

Fibroblast pathology in inflammatory joint disease

The Potential of OMICs Technologies for the Treatment of Immune-Mediated Inflammatory Diseases

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