Serum levels of CD163 and TWEAK in patients with pulmonary arterial hypertension

Jasiewicz, Małgorzata; Kowal, Krzysztof; Kowal-Bielecka, Otylia; Knapp,; Skiepko, Roman; Bodzenta-Łukaszyk, Anna; Sobkowicz, Bożena; Musiał, Włodzimierz J.; Kamiński, Karol

doi:10.1016/j.cyto.2013.12.013

Cited by 31 publications

(19 citation statements)

References 28 publications

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“…Quantification of two-dimensional and Doppler echocardiography data, including right ventricle and atrium dimensions, degree of tricuspid regurgitation and estimation of systolic pulmonary artery pressure (eSPAP) were performed in a standard manner [8]. Systolic function of the right ventricle was assessed by measuring the tricuspid annular plane systolic excursion (TAPSE) and percent fractional area change (FAC).…”

Section: Study Protocolmentioning

confidence: 99%

“…Elevated circulating levels or pulmonary expression of multiple cytokines and chemokines, like IL-1b, IL-6, monocyte chemoattractant protein-1, osteopontin, osteoprotegerin (OPG), receptor activator of nuclear factor kappa B ligand (sRANKL), tumor necrosis factor alpha (TNF-a), sCD163 together with decreased serum levels of sTWEAK, as well as activation and infiltration of the vessel wall with macrophages, T and B lymphocytes and dendritic cells have been documented in patients with PAH [2][3][4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 98%

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Enhanced IL-6 trans-signaling in pulmonary arterial hypertension and its potential role in disease-related systemic damage

et al. 2015

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Section: Study Protocolmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Enhanced IL-6 trans-signaling in pulmonary arterial hypertension and its potential role in disease-related systemic damage

et al. 2015

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“…CD163 is a 130-kDa member of the scavenger receptors and is exclusively expressed by monocytes and macrophages (56). CD163 is a marker for anti-inflammatory activity in macrophages (57) and is potentially a newly identified receptor for TWEAK, as reported previously (18,21). Increasing in vivo and in vitro evidence suggests that the interaction between TWEAK and CD163 may affect the development of atherosclerosis and related diseases (19,20,(57)(58)(59)(60).…”

Section: Cd163: the Second Definite Receptormentioning

confidence: 99%

“…Additionally, the TWEAK/Fn14 combination may become a novel target of interference in atherosclerosis development. As for CD163, in addition to its potential diagnostic uses in atherosclerosis-related diseases, it is also an interesting candidate for medical therapy (19,57,58,60). This is because CD163, as an example of the atheroprotective intraplaque population, eliminates free-Hb and releases a large quantity of anti-inflammatory mediators via activating downstream pathways (62,64).…”

Section: Therapeutic Considerationsmentioning

confidence: 99%

The role of tumor necrosis factor-like weak inducer of apoptosis in atherosclerosis via its two different receptors

Liu

Lin

Xiang

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. At present, it is commonly accepted that atherosclerosis is a chronic inflammatory disease characterized by disorder of the arterial wall. As one of the inflammatory cytokines of the tumor necrosis factor superfamily, tumor necrosis factor-like weak inducer of apoptosis (TWEAK) participates in the formation and progression of atherosclerosis. TWEAK, when binding to its initial receptor, fibroblast growth factor inducible molecule 14 (Fn14), exerts adverse biological functions in atherosclerosis, including dysfunction of endothelial cells, phenotypic change of smooth muscle cells and inflammatory responses of monocytes/macrophages. However, accumulating data supports that, besides Fn14, TWEAK also binds to cluster of differentiation (CD)163, an anti-inflammatory cytokine and a scavenger receptor exclusively expressed by monocytes and macrophages. Furthermore, it has been demonstrated that CD163 is able to internalize TWEAK and likely elicits protective effects in atherosclerosis by terminating inflammation induced by TWEAK. In the present study, the role of TWEAK in atherosclerosis was reviewed, with a predominant focus on CD163 and Fn14 receptors.

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“…In addition, inflammation also plays a key role in PH pathobiology. This is evident from the fact that heightened circulating levels of cytokines, and infiltration of inflammatory cells into the lungs has been observed in patients with PH [7, 10]. However, the focus on inflammatory processes has involved systemic and/or local lung tissue.…”

Section: Introductionmentioning

confidence: 99%

Neuroinflammation in Pulmonary Hypertension: Concept, Facts, and Relevance

et al. 2014

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Pulmonary hypertension (PH) is a progressive lung disease characterized by elevated pressure in the lung vasculature, resulting in right heart failure and premature death. The pathogenesis of PH is complex and multifactorial, involving a dysregulated autonomic nervous system and immune response. Inflammatory mechanisms have been linked to the development and progression of PH; however, these are usually restricted to systemic and/or local lung tissue. Inflammation of the CNS is referred to as neuroinflammation, primarily due to the involvement of “microglia”, the innate immune cells present within the CNS. Microglial activation results in the release of several cytokines and chemokines that trigger neuroinflammation, playing a critical role in the pathogenesis of conditions such as Alzheimer’s, Parkinson’s, hypertension, atherosclerosis, and metabolic disorders. In this review we introduce the concept of neuroinflammation in the context of PH, and discuss possible strategies that could be developed for PH therapy based on this concept.

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Serum levels of CD163 and TWEAK in patients with pulmonary arterial hypertension

Cited by 31 publications

References 28 publications

Enhanced IL-6 trans-signaling in pulmonary arterial hypertension and its potential role in disease-related systemic damage

Enhanced IL-6 trans-signaling in pulmonary arterial hypertension and its potential role in disease-related systemic damage

The role of tumor necrosis factor-like weak inducer of apoptosis in atherosclerosis via its two different receptors

Neuroinflammation in Pulmonary Hypertension: Concept, Facts, and Relevance

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