Therapeutic effects of acetylsalicylic acid in giant cell arteritis (Q28192358)

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Hongyu Yang

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Brian Younge

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Jörg J Goronzy

Giant cell arteritis and Takayasu aortitis: morphologic, pathogenetic and etiologic factors

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language of work or name

English

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publication date

February 2002

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published in

Arthritis & Rheumatology

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volume

46

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page(s)

457-66

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issue

2

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cites work

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Arterial wall injury in giant cell arteritis

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Platelet-derived growth factor, intimal hyperplasia, and ischemic complications in giant cell arteritis.

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Formation of new vasa vasorum in vasculitis. Production of angiogenic cytokines by multinucleated giant cells

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Pathogenic principles in giant cell arteritis

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Correlation of the topographical arrangement and the functional pattern of tissue-infiltrating macrophages in giant cell arteritis

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Glucocorticoid-mediated repression of cytokine gene transcription in human arteritis-SCID chimeras

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Disease patterns and tissue cytokine profiles in giant cell arteritis

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Inhibition of NF-kappa B by sodium salicylate and aspirin

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Antioxidant properties of aspirin: characterization of the ability of aspirin to inhibit silica-induced lipid peroxidation, DNA damage, NF-KB activation, and TNF-alpha production

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Distinct vascular lesions in giant cell arteritis share identical T cell clonotypes

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Functional disruption of the CD28 gene transcriptional initiator in senescent T cells

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Cyclooxygenases: structural, cellular, and molecular biology

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Regulation of interferon-gamma gene expression

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The nuclear factor YY1 suppresses the human gamma interferon promoter through two mechanisms: inhibition of AP1 binding and activation of a silencer element.

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Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs

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The mode of action of aspirin-like drugs: effect on inducible nitric oxide synthase

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Salicylates and sulfasalazine, but not glucocorticoids, inhibit leukocyte accumulation by an adenosine-dependent mechanism that is independent of inhibition of prostaglandin synthesis and p105 of NFkappaB.

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The anti-inflammatory agents aspirin and salicylate inhibit the activity of I(kappa)B kinase-beta

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Inhibition of ultraviolet B-induced activator protein-1 (AP-1) activity by aspirin in AP-1-luciferase transgenic mice

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Cross-talk between steroids and NF-kappa B: what language?

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Immunosuppression by glucocorticoids: inhibition of NF-kappa B activity through induction of I kappa B synthesis

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Role of transcriptional activation of I kappa B alpha in mediation of immunosuppression by glucocorticoids

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Glucocorticoids repress NF-kappaB-driven genes by disturbing the interaction of p65 with the basal transcription machinery, irrespective of coactivator levels in the cell

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Characterization of mechanisms involved in transrepression of NF-kappa B by activated glucocorticoid receptors

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Glucocorticoid-mediated repression of nuclear factor-kappaB-dependent transcription involves direct interference with transactivation

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Methotrexate use in systemic vasculitis

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Use of cytotoxic agents and cyclosporine in the treatment of autoimmune disease. Part 2: Inflammatory bowel disease, systemic vasculitis, and therapeutic toxicity.

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Combined treatment of giant-cell arteritis with methotrexate and prednisone. a randomized, double-blind, placebo-controlled trial

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Treatment of giant cell arteritis: interleukin-6 as a biologic marker of disease activity

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Tissue-Destructive Macrophages in Giant Cell Arteritis

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Tissue cytokine patterns in patients with polymyalgia rheumatica and giant cell arteritis.

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Inhibition of IkappaB kinase activity by sodium salicylate in vitro does not reflect its inhibitory mechanism in intact cells

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The effect of sodium salicylate and aspirin on NF-kappa B

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Interaction of NF-kappaB and NFAT with the interferon-gamma promoter

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Cell-type-specific activation of c-Jun N-terminal kinase by salicylates

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