170: Hypoxia Inducible Factor-1 Preconditioning Protects Transplanted Hearts Against Ischemia-Reperfusion Injury through Effects on Remote Tissues

2010 ◽  
Vol 29 (2) ◽  
pp. S61-S61
Author(s):  
M.A.I. Keranen ◽  
R. Tuuminen ◽  
R. Krebs ◽  
L.A. Flippin ◽  
M. Arend ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1 ◽  
Transplanted Hearts

Erythropoietin Protects the Kidneys Against Ischemia Reperfusion Injury by Activating Hypoxia Inducible Factor-1??

2007 ◽  
Vol 83 (10) ◽  
pp. 1371-1379 ◽  
Author(s):  
Ryoich Imamura ◽  
Toshiki Moriyama ◽  
Yoshitaka Isaka ◽  
Yukiomi Namba ◽  
Naotsugu Ichimaru ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1

scholarly journals Maladaptive Modulations of NLRP3 Inflammasome and Cardioprotective Pathways Are Involved in Diet-Induced Exacerbation of Myocardial Ischemia/Reperfusion Injury in Mice

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Raffaella Mastrocola ◽  
Massimo Collino ◽  
Claudia Penna ◽  
Debora Nigro ◽  
Fausto Chiazza ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Nlrp3 Inflammasome ◽  
Metabolic Diseases ◽  
Ischemia Reperfusion Injury ◽  
Ex Vivo ◽  
Ischemia Reperfusion ◽  
Hypoxia Inducible Factor ◽  
Lactic Dehydrogenase ◽  
Standard Diet ◽  
Myosin Heavy Chain Isoform

Excessive fatty acids and sugars intake is known to affect the development of cardiovascular diseases, including myocardial infarction. However, the underlying mechanisms are ill defined. Here we investigated the balance between prosurvival and detrimental pathways within the heart of C57Bl/6 male mice fed a standard diet (SD) or a high-fat high-fructose diet (HFHF) for 12 weeks and exposed to cardiacex vivoischemia/reperfusion (IR) injury. Dietary manipulation evokes a maladaptive response in heart mice, as demonstrated by the shift of myosin heavy chain isoform content fromαtoβ, the increased expression of the Nlrp3 inflammasome and markers of oxidative metabolism, and the downregulation of the hypoxia inducible factor- (HIF-)2αand members of the Reperfusion Injury Salvage Kinases (RISK) pathway. When exposed to IR, HFHF mice hearts showed greater infarct size and lactic dehydrogenase release in comparison with SD mice. These effects were associated with an exacerbated overexpression of Nlrp3 inflammasome, resulting in marked caspase-1 activation and a compromised activation of the cardioprotective RISK/HIF-2αpathways. The common mechanisms of damage here reported lead to a better understanding of the cross-talk among prosurvival and detrimental pathways leading to the development of cardiovascular disorders associated with metabolic diseases.

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