Inflammasome Activation of Cardiac Fibroblasts Is Essential for Myocardial Ischemia/Reperfusion Injury

By Masanori Kawaguchi, Masafumi Takahashi, Takeki Hata, Y. Kashima, Fumitake Usui, H. Morimoto, A. Izawa, Yasuko Takahashi, J. Masumoto, J. Koyama and 6 more. Circulation, 2011

816 citations recorded by the source corpus.

Subfields: Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/6e899d1d906f2e162e0f9906601b8d23cb32818f

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Citations in the corpus

The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. (2016, background): “cate that inflammasome activation in leukocytes and resident cardiac cells both contribute to ischemic injury.(86) Similarly, isolated perfused NLRP3 murine hearts exhibit reduced”
The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse (2011, background): “Piccini A, et al. (2008) ATP is released by monocytes stimulated with pathogen-sensing receptor ligands and induces IL-1beta and IL-18 secretion in an autocrine way.”
Pathophysiology of Myocardial Infarction (2015, neutral): “pyrin domain 3 (NLRP3) inflammasome in the infarcted myocardium (191, 253), localized in leukocytes, fibroblasts, and border zone cardiomyocytes (191, 253, 315).”
NLRP3 inflammasome: From a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases (2015, neutral): “…. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302 References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 304”