scholarly journals Ginsenoside Rg5 increases cardiomyocyte resistance to ischemic injury through regulation of mitochondrial hexokinase-II and dynamin-related protein 1

2017 ◽  
Vol 8 (2) ◽  
pp. e2625-e2625 ◽  
Author(s):  
Yi-Lin Yang ◽  
Jia Li ◽  
Kang Liu ◽  
Lei Zhang ◽  
Qun Liu ◽  
...  
Keyword(s):  
Ischemic Injury ◽  
Related Protein ◽  
Hexokinase Ii ◽  
Ginsenoside Rg5

scholarly journals Secreted Frizzled Related Protein 4 Reduces Fibrosis Scar Size and Ameliorates Cardiac Function After Ischemic Injury

2010 ◽  
Vol 16 (11) ◽  
pp. 3329-3341 ◽  
Author(s):  
Kentaro Matsushima ◽  
Takashi Suyama ◽  
Chiemi Takenaka ◽  
Naoki Nishishita ◽  
Keiko Ikeda ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Ischemic Injury ◽  
Related Protein ◽  
Scar Size

Astragaloside IV reduces neuronal apoptosis and parthanatos in ischemic injury by preserving mitochondrial hexokinase-II

2019 ◽  
Vol 131 ◽  
pp. 251-263 ◽  
Author(s):  
Ying Li ◽  
Yilin Yang ◽  
Yunpeng Zhao ◽  
Jingmin Zhang ◽  
Baolin Liu ◽  
...  
Keyword(s):  
Neuronal Apoptosis ◽  
Ischemic Injury ◽  
Astragaloside Iv ◽  
Hexokinase Ii

scholarly journals Secreted Frizzled-Related Protein 5 Protects Against Cardiac Rupture and Improves Cardiac Function Through Inhibiting Mitochondrial Dysfunction

2021 ◽  
Vol 8 ◽  
Author(s):  
Xin Huang ◽  
Yan Yan ◽  
Wen Zheng ◽  
Youcai Ma ◽  
Xiao Wang ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Ischemic Injury ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Cardiac Rupture ◽  
Left Ventricular Ejection ◽  
Heart Weight ◽  
Related Protein ◽  
Ampk Activity

Background: Secreted frizzled-related protein 5 (Sfrp5) has been suggested to be a protective regulatory protein in coronary heart disease. However, the role of Sfrp5 in regulating ischemic injury and its consequences is not known. The aim of our study was to explore the effects of Sfrp5 on hearts after myocardial infarction (MI) and to investigate the underlying mechanisms.Methods and Results: We found that Sfrp5 was downregulated over time in the heart tissue of MI mice. To further elucidate the role of Sfrp5 during MI, we established a cardiac overexpression of an Sfrp5 mouse model using the cardiotropic adeno-associated virus serotype 9 (AAV9). Overexpression of Sfrp5 significantly reduced infarct size as demonstrated by a decrease in mortality owing to cardiac rupture. Moreover, cardiac overexpression of Sfrp5 increased left ventricular function and mitochondrial biogenesis, decreased cardiomyocyte apoptosis, suppressed inflammation reaction, inhibited oxidative stress, and ameliorated cardiac remodeling as demonstrated by left ventricular ejection fraction, mitochondrial morphology, heart weight, NADH oxidase activity levels, and myocardial fibrosis at 2 weeks post-MI. At the molecular level, overexpression of Sfrp5 significantly increased the expression of p-AMPKThr172 protein with higher expression of mitochondrial fusion protein (MFN1 and MFN2) and lower expression of mitochondrial fission protein (p-Drp1Ser616/Mid49/MFF/Fis-1). In isolated neonatal rat cardiac myocytes, Sfrp5 treatment attenuated hypoxia-induced mitochondrial dysfunction. Inhibition of AMPK activity with compound C abrogated this benefit.Conclusions: Sfrp5 overexpression inhibits ischemic injury, reduces risk of cardiac rupture, ameliorates post-MI remodeling, and decreases the progression to heart failure via disrupting mitochondrial dysfunction and partly through normalizing the AMPK activity.

scholarly journals Lipoprotein Receptor-Related Protein-6 Protects the Brain From Ischemic Injury

Stroke ◽  
2013 ◽  
Vol 44 (8) ◽  
pp. 2284-2291 ◽  
Author(s):  
T. Abe ◽  
P. Zhou ◽  
K. Jackman ◽  
C. Capone ◽  
B. Casolla ◽  
...  
Keyword(s):  
Ischemic Injury ◽  
Lipoprotein Receptor ◽  
Related Protein ◽  
The Brain ◽  
Lipoprotein Receptor Related Protein

scholarly journals Apelin protects against myocardial ischemic injury by inhibiting dynamin-related protein 1

Oncotarget ◽  
2017 ◽  
Vol 8 (59) ◽  
pp. 100034-100044 ◽  
Author(s):  
Wei Xu ◽  
Hongwei Yu ◽  
Ruixue Ma ◽  
Lina Ma ◽  
Qiushuang Liu ◽  
...  
Keyword(s):  
Ischemic Injury ◽  
Related Protein ◽  
Myocardial Ischemic Injury

C1q/TNF‐related protein‐1 functions to protect against acute ischemic injury in the heart

2015 ◽  
Vol 30 (3) ◽  
pp. 1065-1075 ◽  
Author(s):  
Daisuke Yuasa ◽  
Koji Ohashi ◽  
Rei Shibata ◽  
Naoki Mizutani ◽  
Yoshiyuki Kataoka ◽  
...  
Keyword(s):  
Ischemic Injury ◽  
Related Protein

Abstract 5396: The Role of the Myeloid-Related Protein 8/14 Complex in Postischemic Heart Failure

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Christian Volz ◽  
Felix Lasitschka ◽  
Sebastian N Eichberger ◽  
Ziya Kaya ◽  
Frank Autschbach ◽  
...  
Keyword(s):  
Heart Failure ◽  
Tissue Damage ◽  
Calcium Binding ◽  
Map Kinases ◽  
Ischemic Injury ◽  
Serum Levels ◽  
Ischemic Heart ◽  
Related Protein ◽  
Sustained Activation

The complex formed by two members of the S100 calcium binding protein family, myeloid-related protein complex 8/14 (MRP8/14) exerts pro-inflammatory and pro-apoptotic activity against various cells. Since enhanced MRP8/14 serum levels have recently been associated with acute coronary syndromes (ACS) this study sought to identify the pathophysiological relevance of MRP8/14 in the development and progression of postischemic heart failure (HF). Here we demonstrate that MRP8/14 acts as an early mediator of inflammation and organ damage in I/R injury of the heart via the receptor for advanced glycation end products (RAGE). Wildtype (WT) and RAGE −/− mice were subjected to myocardial infarction by transient ligation of the left anterior descending (LAD) coronary artery and survival, infarction size, cardiac function and remodeling were analyzed up to 4 weeks. Both cardiac RNA and protein levels of MRP8/14 were already elevated 30 minutes after hypoxia in vitro and in ischemic heart with sustained activation up to 28 after ischemic injury. Treatment of mice with recombinant MRP8/14 resulted in increased infarction sizes (70.5±4.5% vs. 57.0±4.3%, n=10, p<0.001) determined after 7 days and reduced cardiac performance in echocardiography after 28 days following I/R injury (18.4±2.1% vs30.6%±3.6, n=10, p<0.001). Moreover treatment with MRP8/14 resulted in an accelerated transition to HF, rapid onset of remodelling and excessive mortality compared to untreated WT-mice with ischemic injury. Signaling studies in isolated ventricles point to the involvement of the MAP kinases JNK, ERK1/2 as well as the nuclear transcription factor NF-κB in ischemic heart failure. Interestingly, infarct size, markers of tissue damage and remodelling were not affected by administration of MRP8/14 in RAGE −/− mice which demonstrated significantly reduced cardiac tissue damage and improved cardiac recovery compared to WT mice. Our novel proof-of- concept study provides evidence that the sustained activation of S100A8/9 critically contributes to the development of postischemic heart failure via RAGE potentially driving the progressive course of patients with HF.

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