Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 121, Issue 5, Pages 1683-1685Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI57748
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Funding
- NHLBI NIH HHS [HL-85534, R01 HL085534, P01 HL071643, R37 HL048129, R37-HL48129, P01-HL71643] Funding Source: Medline
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Proinflammatory stimuli induce inflammation that may progress to sepsis or chronic inflammatory disease. The cytokine TNF-alpha is an important endotoxin-induced inflammatory glycoprotein produced predominantly by macrophages and lymphocytes. TNF-alpha plays a major role in initiating signaling pathways and pathophysiological responses after engaging TNF receptors. In this issue of JCI, Rowlands et al. demonstrate that in lung microvessels, soluble TNF-alpha (sTNF-alpha) promotes the shedding of the TNF-alpha receptor 1 ectodomain via increased mitochond.rial Ca2+ that leads to release of mitochondrial ROS. Shedding mediated by TNF-alpha-converting enzyme (TACE) results in an unattached TNF receptor, which participates in the scavenging of sTNF-alpha, thus limiting the propagation of the inflammatory response. These findings suggest that mitochondrial Ca2+, ROS, and TACE might be therapeutically targeted for treating pulmonary endothelial inflammation.
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