Remote cyclic compression ameliorates myocardial infarction injury in rats via AMPK-dependent pathway

2022 ◽  
pp. 104313
Author(s):  
Senlei Xu ◽  
Xuefeng Xia ◽  
Yuchen Liu ◽  
Fang Chen ◽  
Renjun Gu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cyclic Compression ◽  
Dependent Pathway

scholarly journals Excessive Neutrophil Extracellular Trap Formation Aggravates Acute Myocardial Infarction Injury in Apolipoprotein E Deficiency Mice via the ROS-Dependent Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Zheliang Zhou ◽  
Shuning Zhang ◽  
Suling Ding ◽  
Mieradilijiang Abudupataer ◽  
Zhiwei Zhang ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Apolipoprotein E ◽  
Myocardial Injury ◽  
Early Stage ◽  
Critical Role ◽  
Neutrophil Extracellular Trap ◽  
Coronary Artery Ligation ◽  
Infarct Zone ◽  
Dependent Pathway

Genetically human apolipoprotein E (APOE) ε32 is associated with a decreased risk of ischemic heart disease. ApoE deficiency in mice impairs infarct healing after myocardial infarction (MI). After the ischemic injury, a large number of neutrophils are firstly recruited into the infarct zone and then degrade dead material and promote reparative phase transformation. The role of ApoE in inflammation response in the early stage of MI remains largely unclear. In this study, we investigated the effect of ApoE deficiency on neutrophils’ function and myocardial injury after myocardial infarction. By left coronary artery ligation in ApoE-/- and wild-type (WT) mice, we observed increased infarct size and neutrophil infiltration in ApoE-/- mice. Within the infarct zone, more neutrophil extracellular traps (NETs) were observed in ApoE-/- mice, while increased ex vivo NET formation was detected in ApoE-/- mouse-derived neutrophils through the NADPH oxidase-ROS-dependent pathway. Suppressing overproduced NETs reduced myocardial injury in ApoE-/- mice after ligation. In general, our findings reveal a critical role of apolipoprotein E in regulating Ly6G+ neutrophil activation and NET formation, resulting in limiting myocardial injury after myocardial infarction. In such a process, apolipoprotein E regulates NET formation via the ROS-MAPK-MSK1 pathway.

scholarly journals Sitagliptin decreases ventricular arrhythmias by attenuated glucose-dependent insulinotropic polypeptide (GIP)-dependent resistin signalling in infarcted rats

2016 ◽  
Vol 36 (2) ◽  
Author(s):  
Tsung-Ming Lee ◽  
Wei-Ting Chen ◽  
Nen-Chung Chang
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Arrhythmias ◽  
Sympathetic Innervation ◽  
Dipeptidyl Peptidase ◽  
Phosphatidylinositol 3 Kinase ◽  
Dipeptidyl Peptidase 4 ◽  
Dipeptidyl Peptidase 4 Inhibitor ◽  
Dependent Pathway ◽  
Phosphatidylinositol 3

The rats after myocardial infarction (MI) exposed to sitagliptin, a dipeptidyl peptidase-4 inhibitor, led to attenuated sympathetic innervation probably through a phosphatidylinositol 3-kinase and Akt-dependent pathway.

scholarly journals L5-LDL from ST-elevation myocardial infarction patients induces IL-1β production via LOX-1 and NLRP3 inflammasome activation in macrophages

2017 ◽  
Vol 312 (2) ◽  
pp. H265-H274 ◽  
Author(s):  
Tzu-Ching Yang ◽  
Po-Yuan Chang ◽  
Shao-Chun Lu
Keyword(s):  
Myocardial Infarction ◽  
Inflammatory Cytokine ◽  
Oxidized Ldl ◽  
Ldl Receptor ◽  
Adaptor Protein ◽  
St Segment Elevation ◽  
Segment Elevation Myocardial Infarction ◽  
Caspase 1 ◽  
St Segment ◽  
Dependent Pathway

L5-LDL, the most electronegative LDL associated with major cardiovascular risks, significantly rises in patients with ST-segment elevation myocardial infarction (STEMI). The inflammatory nature of atherosclerotic vascular diseases has prompted us to investigate whether L5-LDL induces the production of inflammatory cytokines, especially vascular ischemia-related interleukin (IL)-1β, in the pathogenesis of STEMI. Clinical data showed that plasma levels of L5-LDL and IL-1β were higher in the STEMI patients than in the controls ( P < 0.05). In THP-1-derived human macrophages, L5-LDL significantly increased the levels of both IL-1β and cleaved caspase-1, indicating the activation of NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasomes by L5-LDL. Knockdown of NLRP3 and its adaptor protein apoptosis-associated speck-like protein containing a CARD (ASC) resulted in decreased L5-LDL-induced IL-1β. Furthermore, knock down of the lectin-type oxidized LDL receptor (LOX-1) in THP-1 cells attenuated L5-LDL-induced activation of NF-κB and caspase-1, leading to subsequent inhibition of IL-1β in macrophages. Furthermore, blockade LOX-1 with neutralizing antibody also inhibited L5-LDL-induced IL-1β in human peripheral blood mononuclear cell-derived macrophages. In conclusion, L5-LDL induces IL-1β production in macrophages by activation of NF-κB and caspase-1 through the LOX-1-dependent pathway. This study represents the evidence linking L5-LDL and the inflammatory cytokine IL-1β in STEMI, and identifies L5-LDL as a novel therapeutic target in acute myocardial infarction. NEW & NOTEWORTHY This study represents the evidence linking L5-LDL and the inflammatory cytokine IL-1β in ST-segment elevation myocardial infarction (STEMI). We elucidate the molecular mechanism underlying L5-LDL-induced production of IL-1β in macrophages. The results showed that L5-LDL induced activation of caspase-1 and NF-κB through the lectin-type oxidized LDL receptor (LOX-1)-dependent pathway, leading to the production of IL-1β.

Myocardial infarction induces sympathetic hyperinnervation via a nuclear factor-κB-dependent pathway in rabbit hearts

2013 ◽  
Vol 535 ◽  
pp. 128-133 ◽  
Author(s):  
Ye Wang ◽  
Fei Suo ◽  
Ju Liu ◽  
Hesheng Hu ◽  
Mei Xue ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Dependent Pathway

scholarly journals 256 Combination of Sonic Hedgehog and a CXCR4 Antagonist improves functional recovery via an MMP-9-dependent Pathway after Myocardial Infarction

2010 ◽  
Vol 2 (1) ◽  
pp. 83
Author(s):  
Jérome Roncalli ◽  
Marie-Ange Renault ◽  
Jorn Tongers ◽  
Tina Thorne ◽  
Sol Misener ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sonic Hedgehog ◽  
Functional Recovery ◽  
Cxcr4 Antagonist ◽  
Dependent Pathway

An electron microscopic study of the intra-myocardial lesions in cases of acute myocardial infarction

1978 ◽  
Vol 36 (2) ◽  
pp. 484-485
Author(s):  
Masahiro Ono ◽  
Kaoru Aihara ◽  
Gompachi Yajima
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Coronary Vessels ◽  
Vascular Wall ◽  
Vascular Changes ◽  
Electron Microscopic ◽  
Main Trunk ◽  
Mechanical Destruction ◽  
Transmission Electron ◽  
Myocardial Lesions

The pathogenesis of the arteriosclerosis in the acute myocardial infarction is the matter of the extensive survey with the transmission electron microscopy in experimental and clinical materials. In the previous communication,the authors have clarified that the two types of the coronary vascular changes could exist. The first category is the case in which we had failed to observe no occlusive changes of the coronary vessels which eventually form the myocardial infarction. The next category is the case in which occlusive -thrombotic changes are observed in which the myocardial infarction will be taken placed as the final event. The authors incline to designate the former category as the non-occlusive-non thrombotic lesions. The most important findings in both cases are the “mechanical destruction of the vascular wall and imbibition of the serous component” which are most frequently observed at the proximal portion of the coronary main trunk.

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