Activation of tumor necrosis factor receptor 1 in airway smooth muscle: a potential pathway that modulates bronchial hyper-responsiveness in asthma?
Citations Over TimeTop 10% of 2000 papers
Abstract
The cellular and molecular mechanisms that are involved in airway hyper-responsiveness are unclear. Current studies suggest that tumor necrosis factor (TNF)-alpha, a cytokine that is produced in considerable quantities in asthmatic airways, may potentially be involved in the development of bronchial hyper-responsiveness by directly altering the contractile properties of the airway smooth muscle (ASM). The underlying mechanisms are not known, but growing evidence now suggests that most of the biologic effects of TNF-alpha on ASM are mediated by the p55 receptor or tumor necrosis factor receptor (TNFR)1. In addition, activation of TNFR1 coupled to the tumor necrosis factor receptor-associated factor (TRAF)2-nuclear factor-kappaB (NF-kappaB) pathway alters calcium homeostasis in ASM, which appears to be a new potential mechanism underlying ASM hyper-responsiveness.
Related Papers
- → Caught in the act: Observation of polymorphonuclear neutrophils for the regulation of tumor necrosis factor-α release by tumor necrosis factor-α converting enzyme in patients with secondary peritonitis*(2005)
- → An important role of tumor necrosis factor-α in the induction of adhesion molecules in psoriasis(乾癬における接着分子発現に対するtumor necrosis factor-αの重要な役割)(1998)
- Effect of rhubarb on tumor necrosis factor,IL-6 and nitric oxide in experimental hepatic necrosis(2004)
- → Tumor Necrosis Factor Therapy(2020)
- → Tumor necrosis factor (TNF); tumor necrosis factor receptor 2 (TNFR2)(2008)