All Relations between nlrp3 and matrix compartment

Publication Sentence Publish Date Extraction Date Species
Wei Gong, Song Mao, Jing Yu, Jiayu Song, Zhanjun Jia, Songming Huang, Aihua Zhan. NLRP3 deletion protects against renal fibrosis and attenuates mitochondrial abnormality in mouse with 5/6 nephrectomy. American journal of physiology. Renal physiology. vol 310. issue 10. 2017-06-27. PMID:26887832. strikingly, tubulointerstitial fibrosis was remarkably attenuated in nlrp3(-/-) mice as evidenced by the blockade of extracellular matrix deposition. 2017-06-27 2023-08-13 mouse
Wentao Liu, Toru Yamashita, Tomoko Kurata, Syoichiro Kono, Nozomi Hishikawa, Kentaro Deguchi, Yun Zhai, Koji Ab. Protective effect of telmisartan on neurovascular unit and inflammasome in stroke-resistant spontaneously hypertensive rats. Neurological research. vol 37. issue 6. 2016-02-29. PMID:25591419. we inspected the effect of telmisartan on the neurovascular unit (nvu) and related inflammatory responses in spontaneously hypertensive rat stroke resistant (shr-sr) by observing the components of nvu such as n-acetyl glucosamine oligomer (nago), collagen iv, astrocytes, and matrix metalloproteinase-9 (mmp-9), as well as inflammasome nod-like receptors family protein 3 (nlrp3). 2016-02-29 2023-08-13 rat
Kathy Triantafilou, Timothy R Hughes, Martha Triantafilou, B Paul Morga. The complement membrane attack complex triggers intracellular Ca2+ fluxes leading to NLRP3 inflammasome activation. Journal of cell science. vol 126. issue Pt 13. 2014-01-16. PMID:23613465. this increase in intracellular ca(2+) concentration leads to ca(2+) accumulation in the mitochondrial matrix via the 'mitochondrial calcium uniporter' (mcu), and loss of mitochondrial transmembrane potential, triggering nlrp3 inflammasome activation and il-1β release. 2014-01-16 2023-08-12 Not clear
Wenjie Wang, Xiangyu Wang, Justin Chun, Akosua Vilaysane, Sharon Clark, Gabrielle French, Nathan A Bracey, Kiril Trpkov, Shirin Bonni, Henry J Duff, Paul L Beck, Daniel A Muruv. Inflammasome-independent NLRP3 augments TGF-β signaling in kidney epithelium. Journal of immunology (Baltimore, Md. : 1950). vol 190. issue 3. 2013-03-26. PMID:23264657. in human and mouse primary renal tecs, nlrp3 expression was increased in response to tgf-β1 stimulation and associated with epithelial-mesenchymal transition (emt) and the expression of α-smooth muscle actin (αsma) and matrix metalloproteinase (mmp) 9. 2013-03-26 2023-08-12 mouse
Robert Zeiser, Olaf Penack, Ernst Holler, Marco Idzk. Danger signals activating innate immunity in graft-versus-host disease. Journal of molecular medicine (Berlin, Germany). vol 89. issue 9. 2011-12-08. PMID:21573893. besides atp, uric acid or soluble extracellular matrix components are functional danger signals that activate the nlrp3 inflammasome when released from dying cells or from extracellular matrix. 2011-12-08 2023-08-12 Not clear
Andrea Babelova, Kristin Moreth, Wasiliki Tsalastra-Greul, Jinyang Zeng-Brouwers, Oliver Eickelberg, Marian F Young, Peter Bruckner, Josef Pfeilschifter, Roland M Schaefer, Hermann-Josef Gröne, Liliana Schaefe. Biglycan, a danger signal that activates the NLRP3 inflammasome via toll-like and P2X receptors. The Journal of biological chemistry. vol 284. issue 36. 2009-10-05. PMID:19605353. our results provide evidence for direct activation of the nlrp3 inflammasome by biglycan and describe a fundamental paradigm of how tissue stress or injury is monitored by innate immune receptors detecting the release of the extracellular matrix components and turning such a signal into a robust inflammatory response. 2009-10-05 2023-08-12 mouse