scholarly journals Thioredoxin1 Inactivation Mediates the Impairment of Ischemia-Induced Angiogenesis and Further Injury in Diabetic Myocardium

2020 ◽  
Vol 57 (2) ◽  
pp. 76-85 ◽  
Author(s):  
Rongrong Hou ◽  
Mingzhi Shen ◽  
Rutao Wang ◽  
Haitao Liu ◽  
Chao Gao ◽  
...  
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2006 ◽  
Vol 6 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Thomas H. Marwick
Keyword(s):  

2018 ◽  
Vol 25 (14) ◽  
pp. 1463-1481 ◽  
Author(s):  
Feyzizadeh Saeid ◽  
Javadi Aniseh ◽  
Badalzadeh Reza ◽  
Vafaee S Manouchehr

Ischaemic heart diseases are one of the major causes of death in the world. In most patients, ischaemic heart disease is coincident with other risk factors such as diabetes. Patients with diabetes are more prone to cardiac ischaemic dysfunctions including ischaemia–reperfusion injury. Ischaemic preconditioning, postconditioning and remote conditionings are reliable interventions to protect the myocardium against ischaemia–reperfusion injuries through activating various signaling pathways and intracellular mediators. Diabetes can disrupt the intracellular signaling cascades involved in these myocardial protections, and studies have revealed that cardioprotective effects of the conditioning interventions are diminished in the diabetic condition. The complex pathophysiology and poor prognosis of ischaemic heart disease among people with diabetes necessitate the investigation of the interaction of diabetes with ischaemia–reperfusion injury and cardioprotective mechanisms. Reducing the outcomes of ischaemia–reperfusion injury using targeted strategies would be particularly helpful in this population. In this study, we review the protective interventional signaling pathways and mediators which are activated by ischaemic conditioning strategies in healthy and diabetic myocardium with ischaemia–reperfusion injury.


2018 ◽  
Vol 123 (Suppl_1) ◽  
Author(s):  
Vahid Agbortoko ◽  
Yuhong Liu ◽  
Guangbin Shi ◽  
Anny Usheva ◽  
Arun K Singh ◽  
...  
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2019 ◽  
Vol 33 (6) ◽  
pp. 669-674 ◽  
Author(s):  
Mitchel Tate ◽  
Gavin C. Higgins ◽  
Miles J. De Blasio ◽  
Runa Lindblom ◽  
Darnel Prakoso ◽  
...  

Abstract Purpose Methylglyoxal, a by-product of glycolysis and a precursor in the formation of advanced glycation end-products, is significantly elevated in the diabetic myocardium. Therefore, we sought to investigate the mitochondria-targeted methylglyoxal scavenger, MitoGamide, in an experimental model of spontaneous diabetic cardiomyopathy. Methods Male 6-week-old Akita or wild type mice received daily oral gavage of MitoGamide or vehicle for 10 weeks. Several morphological and systemic parameters were assessed, as well as cardiac function by echocardiography. Results Akita mice were smaller in size than wild type counterparts in terms of body weight and tibial length. Akita mice exhibited elevated blood glucose and glycated haemoglobin. Total heart and individual ventricles were all smaller in Akita mice. None of the aforementioned parameters was impacted by MitoGamide treatment. Echocardiographic analysis confirmed that cardiac dimensions were smaller in Akita hearts. Diastolic dysfunction was evident in Akita mice, and notably, MitoGamide treatment preferentially improved several of these markers, including e′/a′ ratio and E/e′ ratio. Conclusions Our findings suggest that MitoGamide, a novel mitochondria-targeted approach, offers cardioprotection in experimental diabetes and therefore may offer therapeutic potential for the treatment of cardiomyopathy in patients with diabetes.


2020 ◽  
Vol 320 ◽  
pp. 106-111
Author(s):  
Elias Björnson ◽  
Ylva Östlund ◽  
Marcus Ståhlman ◽  
Martin Adiels ◽  
Elmir Omerovic ◽  
...  

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