AK003290 Protects Myocardial Cells Against Apoptosis and Promotes Cardiac Function Recovery Via miR-539-3p/ErbB4 Axis in Ischemic-Reperfusion Injury

2021 ◽  
Vol 40 (12) ◽  
pp. 1528-1538
Author(s):  
Yong Tang ◽  
Yan Tang ◽  
Yin Xiang ◽  
Jianhua Yan ◽  
Kai Guo
Keyword(s):  
Cardiac Function ◽  
Reperfusion Injury ◽  
Myocardial Cells ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Function Recovery

Abstract 342: Increased Myocardial Ischemic/Reperfusion Injury in Renal Failure Involves Cardiac Adiponectin Signal Deficiency

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Ling Tao ◽  
Yanbin Song ◽  
Junyi Zhang ◽  
Weidong Huang ◽  
Yi Liu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Renal Failure ◽  
Cardiac Function ◽  
Infarct Size ◽  
Reperfusion Injury ◽  
Tunel Staining ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Nitrative Stress ◽  
Cardiovascular Morbidity And Mortality

Chronic kidney disease (CKD) is associated with increased incidence as well as adverse outcomes of acute myocardial infarction. Adiponectin (APN), known as a cardioprotective factor, has been observed decreased in cardiovascular disorders including myocardial infarction. However, plasma APN levels are significantly increased and are inversely related to the risk of cardiovascular morbidity and mortality in patients with CKD. The mechanism underlying the paradoxical relationship between high APN and poor cardiac outcome remains unclear. In the present study, subtotal nephrectomized (SN) and sham-operated mice were randomly subjected to a 30 min myocardial ischemia followed by 24 hrs reperfusion with or without human recombinant gAd treatment (2μg/g/d, 7days). Compared with sham WT mice, SN mice displayed significantly depressed cardiac function and enlarged infarct size following MI/R. TUNEL staining and caspase-3 activity assay demonstrated markedly increased cardiomyocyte apoptosis in SN mice following MI/R. What’s more, increased plasma total APN levels was observed in SN mice 4 weeks after MI/R. Importantly, SN caused further decreased cardiac function and larger infarct size in APN knockout (KO) mice compared with those in SN WT mice subjected to MI/R. However, gAd treatment significantly enhanced cardiac function and reduced infarct size and apoptosis in both WT and KO mice. Further, we found that SN KO mice showed more reduced eNOS phosphorylation, upregulated iNOS expression and ·O 2 - production and consequently increased peroxynitrite production in cardiac tissue than SN WT animals, which can be partly reversed by administration of gAd. AdipoR1 expression was reduced 4-wk after SN whereas AdipoR2 showed no significant change. More importantly, AMPK activation was also inhibited after SN and exogenous gAd supplementation reversed this change. In conclusion, the present study demonstrates that renal dysfunction increases cardiac susceptibility to ischemic/reperfusion injury, which is associated with downregulated APN/AdipoR1/AMPK signaling and increased oxidative/nitrative stress in local myocardium, and provides the first evidence for the benefits of exogenous supplement of APN on cardiac outcomes in renal failure.

The Effect of C1 Esterase Inhibitor on Ischemic Reperfusion Injury in Rat Epigastric Skin Flaps: Preliminary Results

2014 ◽  
Vol 30 (S 01) ◽  
Author(s):  
Inmaculada Jurado ◽  
Alberto Rodríguez ◽  
Carmen Vázquez ◽  
Víctor Velasco ◽  
Víctor Turrión ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Skin Flaps ◽  
Ischemic Reperfusion Injury ◽  
Preliminary Results ◽  
C1 Esterase Inhibitor ◽  
Ischemic Reperfusion ◽  
Esterase Inhibitor

Myocardial Ischemic-reperfusion Injury in a Rat Model of Metabolic Syndrome

Obesity ◽  
2008 ◽  
Vol 16 (10) ◽  
pp. 2253-2258 ◽  
Author(s):  
Mahmood S. Mozaffari ◽  
Stephen W. Schaffer
Keyword(s):  
Metabolic Syndrome ◽  
Reperfusion Injury ◽  
Rat Model ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion

scholarly journals Role of NAD(P)H Oxidase- and Mitochondria-Derived Reactive Oxygen Species in Cardioprotection of Ischemic Reperfusion Injury by Angiotensin II

Hypertension ◽  
2005 ◽  
Vol 45 (5) ◽  
pp. 860-866 ◽  
Author(s):  
Shoji Kimura ◽  
Guo-Xing Zhang ◽  
Akira Nishiyama ◽  
Takatomi Shokoji ◽  
Li Yao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Reperfusion Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion

Abstract 90: Diabetes Impairs Post-stroke Cerebrovascular Plasticity And Long-term Functional Recovery.

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Roshini Prakash ◽  
Weiguo Li ◽  
Zhi Qu ◽  
Susan C Fagan ◽  
Adviye Ergul
Keyword(s):  
Cognitive Decline ◽  
Reperfusion Injury ◽  
Functional Recovery ◽  
Diabetic Rats ◽  
Neurological Deficits ◽  
Ischemic Reperfusion Injury ◽  
Post Stroke ◽  
Ischemic Reperfusion ◽  
Sensorimotor Recovery ◽  
The Impact

Background: Stroke associated with pre-existing diabetes worsens ischemic injury and impairs recovery. We have previously shown that type-2-diabetic rats subjected to cerebral ischemic reperfusion injury develop hemorrhagic transformation (HT) and greater neurological deficits. These diabetic rats also exhibit enhanced dysfunctional cerebral neovascularization that increases the risk of bleeding post-stroke. However, our knowledge of vascular and functional plasticity during the recovery phase of diabetic stroke is limited. This study tested the hypothesis that post-stroke neovascularization is impaired in diabetes and this is associated with poor sensorimotor and cognitive outcomes. Methods: Reparative neovascularization was assessed in the lesional and non-lesional areas in diabetic rats after 14 days of ischemic reperfusion injury. 3-dimensional reconstruction of the FITC stained vasculature were obtained by confocal microscopy and stereological parameters including vascular volume and surface area were measured. Astrogliosis was also determined by GFAP staining. The relative rates of sensorimotor recovery, cognitive decline and spontaneous activity were assessed. Results: Diabetes impairs reparative neovascularization in the lesional areas compared to control rats. Astroglial swelling and reactivity was pronounced in diabetic stroke compared to control stroke. Rate of sensorimotor recovery was significantly slower in diabetic stroke compared to the controls. Diabetes also exacerbated anxiety-like symptoms and cognitive decline post-stroke relative to control. Conclusion: Diabetes impairs post-stroke reparative neovascularization and impedes functional recovery. The impact of glycemic control on poor recovery in this critical period needs to be tested. N=6-8 * p≤ 0.05, ** p≤ 0.005

Double-Negative αβ T cells: A Novel Player in Lung Ischemic-Reperfusion Injury

2018 ◽  
Vol 37 (4) ◽  
pp. S221
Author(s):  
J. Hsu ◽  
A. Krishnan ◽  
S. Lee ◽  
J.M. Dodd-o ◽  
B. Kim ◽  
...  
Keyword(s):  
T Cells ◽  
Reperfusion Injury ◽  
Double Negative ◽  
Ischemic Reperfusion Injury ◽  
Ischemic Reperfusion ◽  
Αβ T Cells
Sign in / Sign up

Export Citation Format

Share Document