| 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 |