2020
DOI: 10.1007/s10863-020-09832-w
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MiR-703 protects against hypoxia/reoxygenation-induced cardiomyocyte injury via inhibiting the NLRP3/caspase-1-mediated pyroptosis

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Cited by 18 publications
(36 citation statements)
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“…Programmed necrosis mainly contains necroptosis, mitochondrial permeability transition‐associated necrosis, ferroptosis and pyroptosis 7,35,36 . Currently, myocardial pyroptosis is considered to be one of the pivotal pathogenetic mechanisms of MIRI and has drawn considerable attentions during MIRI 6,7,10,11,36 . Pyroptosis acts as a pro‐inflammatory cell death and was characterized as NLRP3‐caspase‐1‐dependent response 6,7,10,11,36 .…”
Section: Discussionmentioning
confidence: 99%
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“…Programmed necrosis mainly contains necroptosis, mitochondrial permeability transition‐associated necrosis, ferroptosis and pyroptosis 7,35,36 . Currently, myocardial pyroptosis is considered to be one of the pivotal pathogenetic mechanisms of MIRI and has drawn considerable attentions during MIRI 6,7,10,11,36 . Pyroptosis acts as a pro‐inflammatory cell death and was characterized as NLRP3‐caspase‐1‐dependent response 6,7,10,11,36 .…”
Section: Discussionmentioning
confidence: 99%
“…MIRI affects clinical efficacy of revascularization strategies and serves as an important factor in worsening heart structure and function 1‐3,6,7 . Although programmed cell death that mainly contains necrosis, apoptosis and autophagy acts as the major pathogenesis in the development of MIRI, 3,8,9 it is now verified that pyroptosis‐associated necrosis also plays important roles in MIRI 6,7,10 …”
Section: Introductionmentioning
confidence: 99%
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