2014
DOI: 10.1536/ihj.14-140
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Letter by Mezzaroma, <i>et al</i> Regarding Article, “NLRP3 Inflammasome as a Therapeutic Target in Myocardial Infarction”

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Cited by 7 publications
(2 citation statements)
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“…Inhibiting inflammasome formation limits infarct size and cardiac remodelling after MI. 33,36 Interestingly, the MI-induced up-regulation of cytokines and genes related to inflammasome signalling (see Supplementary material online, Figure S13) was augmented in Hspb1 À/À mice. Taken together, our data suggest a cardiomyocyte-specific role for HSPB1 in the recruitment of leucocytes in MI hearts.…”
Section: Discussionmentioning
confidence: 99%
“…Inhibiting inflammasome formation limits infarct size and cardiac remodelling after MI. 33,36 Interestingly, the MI-induced up-regulation of cytokines and genes related to inflammasome signalling (see Supplementary material online, Figure S13) was augmented in Hspb1 À/À mice. Taken together, our data suggest a cardiomyocyte-specific role for HSPB1 in the recruitment of leucocytes in MI hearts.…”
Section: Discussionmentioning
confidence: 99%
“…Ωστόσο, τα μυοκαρδιακά κύτταρα δεν εκκρίνουν σταθερά υψηλά επίπεδα IL-1β. Παρόλα αυτά, ο σχηματισμός του NLRP3 φλεγμονοσώματος σε αυτά τα κύτταρα ενεργοποιεί την κασπάση-1 και επάγει την πυρόπτωση (εικόνα 10)[330,331]. Ο NLRP3 δεν είναι ο μόνος υποδοχέας που μπορεί να ενεργοποιήσει την κασπάση-1 και ως εκ τούτου να επάγει την έκφραση της IL-1β και της IL-18.…”
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