Current Updates on Potential Role of Flavonoids in Hypoxia/Reoxygenation Cardiac Injury Model

2021 ◽  
Author(s):  
Shafreena Shaukat Ali ◽  
Liza Noordin ◽  
Ruzilawati Abu Bakar ◽  
Satirah Zainalabidin ◽  
Zakiah Jubri ◽  
...  
Keyword(s):  
Potential Role ◽  
Cardiac Injury ◽  
Injury Model ◽  
Hypoxia Reoxygenation

scholarly journals Potential Role of Nuclear FactorκB in Diabetic Cardiomyopathy

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
O. Lorenzo ◽  
B. Picatoste ◽  
S. Ares-Carrasco ◽  
E. Ramírez ◽  
J. Egido ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Transcription Factor ◽  
Diabetic Cardiomyopathy ◽  
Nuclear Factor Kappa B ◽  
Potential Role ◽  
Heart Diseases ◽  
Cardiac Injury ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa

Diabetic cardiomyopathy entails the cardiac injury induced by diabetes independently of any vascular disease or hypertension. Some transcription factors have been proposed to control the gene program involved in the setting and development of related processes. Nuclear factor-kappa B is a pleiotropic transcription factor associated to the regulation of many heart diseases. However, the nuclear factor-kappa B role in diabetic cardiomyopathy is under investigation. In this paper, we review the nuclear factor-kappa B pathway and its role in several processes that have been linked to diabetic cardiomyopathy, such as oxidative stress, inflammation, endothelial dysfunction, fibrosis, hypertrophy and apoptosis.

scholarly journals Potential Role of Axonal Chemorepellent Slit2 in Modulating Adventitial Inflammation in a Rat Carotid Artery Balloon Injury Model

2016 ◽  
Vol 67 (5) ◽  
pp. 433-441 ◽  
Author(s):  
Dong Liu ◽  
Yan Xiao ◽  
Romesh R. Subramanian ◽  
Ei-ichi Okamoto ◽  
Josiah N. Wilcox ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Potential Role ◽  
Balloon Injury ◽  
Injury Model

Inhibition of sphingomyelin synthase 2 relieves hypoxia-induced cardiomyocyte injury by reinforcing Nrf2/ARE activation via modulation of GSK-3β

2020 ◽  
pp. 096032712096995
Author(s):  
Aiping Jin ◽  
Haijuan Cheng ◽  
Lina Xia ◽  
Sha Ye ◽  
Cuiling Yang
Keyword(s):  
Myocardial Infarction ◽  
Potential Role ◽  
Glycogen Synthase ◽  
Tissue Injury ◽  
Cardiac Injury ◽  
Ros Generation ◽  
Related Factor ◽  
Loss Of Function ◽  
Sphingomyelin Synthase

Sphingomyelin synthase 2 (SMS2) is a vital contributor to tissue injury and affects various pathological processes. However, whether SMS2 participates in the modulation of cardiac injury in myocardial infarction has not been determined. This study aimed to evaluate the potential role of SMS2 in the regulation of cardiomyocyte injury induced by hypoxia, an in vitro model for studying myocardial infarction. Our data revealed that SMS2 expression was significantly upregulated in cardiomyocytes in response to hypoxia. Loss-of-function experiments revealed that knockdown of SMS2 markedly restored the viability of cardiomyocytes impaired by hypoxia, and attenuated hypoxia-evoked apoptosis and reactive oxygen species (ROS) generation. In contrast, cardiomyocytes that highly expressed SMS2 were more sensitive to hypoxia-induced injury. Moreover, SMS2 deficiency enhanced the activation of nuclear factor erythroid 2-related factor 2 (Nrf2) signaling through inactivation of glycogen synthase kinase-3β. Notably, suppression of Nrf2 markedly abrogated SMS2 knockdown-mediated cardioprotective effects on hypoxia-exposed cardiomyocytes. Our results illustrate that downregulation of SMS2 exerts a cardioprotective function by protecting cardiomyocytes from hypoxia-induced apoptosis and oxidative stress through enhancement of Nrf2 activation. Our study indicates a potential role of SMS2 in the modulation of cardiac injury, which may contribute to the progression of myocardial infarction.

scholarly journals Circular RNA ciRs-126 promotes hypoxia/reoxygenation cardiac injury possibly through miR-21

2022 ◽  
Vol 20 (1) ◽  
Author(s):  
Changming Tan ◽  
Jianming Li ◽  
Zhaoshun Yuan ◽  
Yongxin Mu
Keyword(s):  
Cell Apoptosis ◽  
Cardiac Injury ◽  
Circular Rna ◽  
Healthy Controls ◽  
Plasma Samples ◽  
Inhibitory Effects ◽  
Apoptosis Assay ◽  
Induced Apoptosis ◽  
Hypoxia Reoxygenation

Abstract Background This study aimed to analyze the role of circular RNA ciRs-126 in hypoxia/reoxygenation cardiac injury (H/R). Methods Expression of ciRs-126 and miR-21 in plasma samples from patients with H/R and healthy controls was determined by RT-qPCR. Correlations were analyzed by linear regression. Overexpression of ciRs-126 and miR-21 was achieved in cardiomyocytes to explore their crosstalk. The roles of ciRs-126 and miR-21 in H/R-induced apoptosis of cardiomyocytes were analyzed using cell apoptosis assay. Results CiRs-126 was upregulated and miR-21 was downregulated in H/R patients. They were inversely correlated across plasma samples from H/R patients. In H/R cardiomyocytes, ciRs-126 was upregulated and miR-21 was downregulated. In cardiomyocytes, ciRs-126 overexpression decreased miR-21 level and reduced the inhibitory effects of miR-21 overexpression on H/R-induced cell apoptosis. Conclusions Circular RNA ciRs-126 may suppress miR-21 expression to promote H/R cardiac injury.

scholarly journals The adipokine Retnla deficiency increases responsiveness to cardiac repair through adiponectin-rich bone marrow cells

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Yong Sook Kim ◽  
Hyang Hee Cho ◽  
Dong Im Cho ◽  
Hye-yun Jeong ◽  
Soo yeon Lim ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Cardiac Function ◽  
Bone Marrow Cells ◽  
Cardiac Fibroblasts ◽  
Cardiac Injury ◽  
Bone Marrow Niche ◽  
Injury Model ◽  
Transfer Study ◽  
Marrow Cells

AbstractResistin-like alpha (Retnla) is a member of the resistin family and known to modulate fibrosis and inflammation. Here, we investigated the role of Retnla in the cardiac injury model. Myocardial infarction (MI) was induced in wild type (WT), Retnla knockout (KO), and Retnla transgenic (TG) mice. Cardiac function was assessed by echocardiography and was significantly preserved in the KO mice, while worsened in the TG group. Angiogenesis was substantially increased in the KO mice, and cardiomyocyte apoptosis was markedly suppressed in the KO mice. By Retnla treatment, the expression of p21 and the ratio of Bax to Bcl2 were increased in cardiomyocytes, while decreased in cardiac fibroblasts. Interestingly, the numbers of cardiac macrophages and unsorted bone marrow cells (UBCs) were higher in the KO mice than in the WT mice. Besides, phosphorylated histone H3(+) cells were more frequent in bone marrow of KO mice. Moreover, adiponectin in UBCs was notably higher in the KO mice compared with WT mice. In an adoptive transfer study, UBCs were isolated from KO mice to transplant to the WT infarcted heart. Cardiac function was better in the KO-UBCs transplanted group in the WT-UBCs transplanted group. Taken together, proliferative and adiponectin-rich bone marrow niche was associated with substantial cardiac recovery by suppression of cardiac apoptosis and proliferation of cardiac fibroblast.

POPDC proteins and cardiac function

2019 ◽  
Vol 47 (5) ◽  
pp. 1393-1404 ◽  
Author(s):  
Thomas Brand
Keyword(s):  
Potential Role ◽  
Striated Muscle ◽  
Short Review ◽  
Effector Proteins ◽  
Muscle Disease ◽  
Disease Genes ◽  
Protein Protein Interaction ◽  
Interaction Partners ◽  
And Function

Abstract The Popeye domain-containing gene family encodes a novel class of cAMP effector proteins in striated muscle tissue. In this short review, we first introduce the protein family and discuss their structure and function with an emphasis on their role in cyclic AMP signalling. Another focus of this review is the recently discovered role of POPDC genes as striated muscle disease genes, which have been associated with cardiac arrhythmia and muscular dystrophy. The pathological phenotypes observed in patients will be compared with phenotypes present in null and knockin mutations in zebrafish and mouse. A number of protein–protein interaction partners have been discovered and the potential role of POPDC proteins to control the subcellular localization and function of these interacting proteins will be discussed. Finally, we outline several areas, where research is urgently needed.

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