Rosuvastatin protects against coronary microembolization-induced cardiac injury via inhibiting NLRP3 inflammasome activation

• Published in: Cell death & disease Vol. 12; no. 1; p. 78
• Main Authors: Chen, Ao, Chen, Zhangwei, Zhou, You, Wu, Yuan, Xia, Yan, Lu, Danbo, Fan, Mengkang, Li, Su, Chen, Jinxiang, Sun, Aijun, Zou, Yunzeng, Qian, Juying, Ge, Junbo
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 12.01.2021; Springer Nature B.V; Nature Publishing Group
• Subjects: 13/1; 13/31; 14/34; 631/80/82; 692/699/75; 82/58; 82/80; Animals; Antibodies; Anticholesteremic Agents - pharmacology; Anticholesteremic Agents - therapeutic use; Apoptosis; Biochemistry; Biomedical and Life Sciences; Caspase-1; Cell Biology; Cell Culture; Cell viability; Dehydrogenases; Disease; Energy metabolism; Fibrosis; Heart; Hospitals; Humans; Hypoxia; IL-1β; Immunology; Inflammasomes; Inflammasomes - metabolism; L-Lactate dehydrogenase; Lactic acid; Life Sciences; Male; Mice; Mitochondria; Molecular modelling; Muscle contraction; Myocardial infarction; Myocardial Reperfusion Injury - drug therapy; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism; Oxidative metabolism; Oxidative phosphorylation; Pathogenesis; Phosphorylation; Propidium iodide; Proteins; Proteomics; Pyroptosis; Reactive oxygen species; Rosuvastatin Calcium - pharmacology; Rosuvastatin Calcium - therapeutic use; Statins; Tumor necrosis factor-TNF; Tumor necrosis factor-α

Coronary microembolization (CME), a common reason for periprocedural myocardial infarction (PMI), bears very important prognostic implications. However, the molecular mechanisms related to CME remain largely elusive. Statins have been shown to prevent PMI, but the underlying mechanism has not been i...