Giant Cell Arteritis and Angiogenesis: A Review

Mitchell, Ellen Browne; Cestari, Dean M.

doi:10.1080/08820530902805776

Cited by 6 publications

(3 citation statements)

References 25 publications

(38 reference statements)

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“…Chronic GCA requires T-cells persisting in the arterial wall; to orchestrate macrophage activation, drive inflammation-associated neo-angiogenesis and promote intimal hyperplasia 26,27 . Current therapies focus on pro-inflammatory innate cytokines 28,29 , but fail to eliminate wall-infiltrating T-cells 2 .…”

Section: Introductionmentioning

confidence: 99%

Inhibition of JAK-STAT Signaling Suppresses Pathogenic Immune Responses in Medium and Large Vessel Vasculitis

Zhang¹,

Watanabe²,

Berry³

et al. 2018

Circulation

173

145

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Section: Introductionmentioning

confidence: 99%

Inhibition of JAK-STAT Signaling Suppresses Pathogenic Immune Responses in Medium and Large Vessel Vasculitis

Zhang¹,

Watanabe²,

Berry³

et al. 2018

Circulation

173

145

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“…Vasa vasorum neongiogenesis is typical of large vessel vasculitides [ 11 , 12 ]. Inflammatory cells infiltrate vasculitic lesions through vasa vasorum, and neoangiogenesis within arterial lesions have been associated with histologic features, such as disruption of the internal elastic membrane and intimal hyperplasia, which is thought to cause stenosis [ 11 , 30 ]. The CgA system modulates neoangiogenesis [ 15 , 17 ] and fibroblast adhesion, endothelial and VSMC proliferation and migration, and endothelial response to inflammatory stimuli.…”

Section: Discussionmentioning

confidence: 99%

Chromogranin-A production and fragmentation in patients with Takayasu arteritis

et al. 2016

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BackgroundChromogranin-A (CgA) is a secretory protein processed into peptides that regulate angiogenesis and vascular cells activation, migration and proliferation. These processes may influence arterial inflammation and remodelling in Takayasu arteritis (TA).MethodsPlasma levels of full-length CgA (CgA439), CgA fragments lacking the C-terminal region (CgA-FRs) and the N-terminal fragment, CgA1–76 (vasostatin-1, VS-1) were analysed in 42 patients with TA and 20 healthy age-matched controls. Vascular remodelling was longitudinally assessed by imaging. CgA peptides were related to markers of systemic and local inflammation, disease activity and vascular remodelling.ResultsLevels of CgA-FRs and VS-1 were increased in TA. Treatment with proton-pump inhibitors (PPIs) and arterial hypertension partially accounted for CgA levels and high inter-patient variability. CgA439, CgA-FRs and VS-1 levels did not reflect disease activity or extent. Markers of systemic or local inflammation correlated with higher CgA-FRs and VS-1 in normotensive patients and with higher CgA439 in hypertensive patients. Treatment with non-biologic anti-rheumatic agents was associated with increased CgA-FRs and a distinctive regulation of CgA processing. Reduced blood levels of anti-angiogenic CgA peptides were associated with vascular remodelling in the groups of patients on PPIs and with arterial hypertension.ConclusionsThe plasma levels of CgA fragments are markedly increased in TA as a consequence of disease- and therapy-related variables. Anti-angiogenic forms of CgA may limit vascular remodelling. Given the effect of the various CgA peptides, it is advisable to limit the therapeutic prescriptions that might influence CgA-derived peptide levels to clearly agreed medical indications until further data become available.Electronic supplementary materialThe online version of this article (doi:10.1186/s13075-016-1082-2) contains supplementary material, which is available to authorized users.

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“…The ischaemic process is presumably due to luminal stenosis from hyperplasia, initiated and promoted by various inflammatory and pro-angiogenic factors (13). It usually presents as a sudden onset of painless unilateral or bilateral loss of vision.…”

Section: What Are the Features To Look For In A Patient With Suspectementioning

confidence: 99%

Giant Cell Arteritis– Who to Refer to?

Lim¹,

Ey²,

Strang³

et al. 2015

West Indian Med J

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Giant cell arteritis is a systemic immune-mediated vasculitis affecting the medium and large arteries. Typical symptoms include new headache, jaw claudication, tender temporal artery, polymyalgia rheumatica, fever and anorexia. Visual loss resulting from giant cell arteritis is an ophthalmic emergency and requires immediate assessment and referral to the ophthalmologist for prompt treatment with steroids. This article provides a systematic approach to the diagnosis and management of giant cell arteritis.

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Giant Cell Arteritis and Angiogenesis: A Review

Cited by 6 publications

References 25 publications

Inhibition of JAK-STAT Signaling Suppresses Pathogenic Immune Responses in Medium and Large Vessel Vasculitis

Inhibition of JAK-STAT Signaling Suppresses Pathogenic Immune Responses in Medium and Large Vessel Vasculitis

Chromogranin-A production and fragmentation in patients with Takayasu arteritis

Giant Cell Arteritis– Who to Refer to?

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