Circular RNA Foxo3 Relieves Myocardial Ischemia/Reperfusion Injury by Suppressing Autophagy via Inhibiting HMGB1 by Repressing KAT7 in Myocardial Infarction
出版年份 2021 全文链接
标题
Circular RNA Foxo3 Relieves Myocardial Ischemia/Reperfusion Injury by Suppressing Autophagy via Inhibiting HMGB1 by Repressing KAT7 in Myocardial Infarction
作者
关键词
-
出版物
Journal of Inflammation Research
Volume Volume 14, Issue -, Pages 6397-6407
出版商
Informa UK Limited
发表日期
2021-11-30
DOI
10.2147/jir.s339133
参考文献
相关参考文献
注意:仅列出部分参考文献,下载原文获取全部文献信息。- Circular RNA circRHOT1 contributes to pathogenesis of non-small cell lung cancer by epigenetically enhancing C-MYC expression through recruiting KAT5
- (2021) Xiaoyan Ren et al. Aging-US
- Silencing of circFoxO3 Protects HT22 Cells from Glutamate-Induced Oxidative Injury via Regulating the Mitochondrial Apoptosis Pathway
- (2020) Shao-Peng Lin et al. CELLULAR AND MOLECULAR NEUROBIOLOGY
- CircFOXO3 rs12196996, a polymorphism at the gene flanking intron, is associated with circFOXO3 levels and the risk of coronary artery disease
- (2020) Yu-Lan Zhou et al. Aging-US
- CircFOXO3 functions as a molecular sponge for miR-143-3p to promote the progression of gastric carcinoma via upregulating USP44
- (2020) Tian Xiang et al. GENE
- High-dose intramyocardial HMGB1 induces long-term cardioprotection in sheep with myocardial infarction
- (2019) María del Rosario Bauzá et al. Drug Delivery and Translational Research
- Atorvastatin Enhances the Therapeutic Efficacy of Mesenchymal Stem Cells Derived Exosomes in Acute Myocardial Infarction via Up-regulating Long Non-coding RNA H19
- (2019) Peisen Huang et al. CARDIOVASCULAR RESEARCH
- Circular RNA Ttc3 regulates cardiac function after myocardial infarction by sponging miR-15b
- (2019) Lidong Cai et al. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
- Resolvin D1 Attenuates Myocardial Infarction in a Rodent Model with the Participation of the HMGB1 Pathway
- (2019) Rui Liu et al. CARDIOVASCULAR DRUGS AND THERAPY
- Loss of Super-Enhancer-Regulated circRNA Nfix Induces Cardiac Regeneration After Myocardial Infarction in Adult Mice
- (2019) Senlin Huang et al. CIRCULATION
- High Mobility Group Box-1 (HMGB1): A potential target in therapeutics
- (2019) Eyaldeva C. Vijayakumar et al. CURRENT DRUG TARGETS
- TLR9 is essential for HMGB1-mediated post-myocardial infarction tissue repair through affecting apoptosis, cardiac healing, and angiogenesis
- (2019) Fang-Yuan Liu et al. Cell Death & Disease
- CircFOXO3 promotes glioblastoma progression by acting as a competing endogenous RNA for NFAT5
- (2019) Shuai Zhang et al. NEURO-ONCOLOGY
- Circular RNA CircFndc3b modulates cardiac repair after myocardial infarction via FUS/VEGF-A axis
- (2019) Venkata Naga Srikanth Garikipati et al. Nature Communications
- Extracellular HMGB1 as a therapeutic target in inflammatory diseases
- (2018) Ulf Andersson et al. EXPERT OPINION ON THERAPEUTIC TARGETS
- The circular RNA ACR attenuates myocardial ischemia/reperfusion injury by suppressing autophagy via modulation of the Pink1/ FAM65B pathway
- (2018) Lu-Yu Zhou et al. CELL DEATH AND DIFFERENTIATION
- The Endotoxin Delivery Protein HMGB1 Mediates Caspase-11-Dependent Lethality in Sepsis
- (2018) Meihong Deng et al. IMMUNITY
- Acute myocardial infarction
- (2017) Grant W Reed et al. LANCET
- Acute Myocardial Infarction
- (2017) Jeffrey L. Anderson et al. NEW ENGLAND JOURNAL OF MEDICINE
- Antioxidant nanomaterials in advanced diagnoses and treatments of ischemia reperfusion injuries
- (2017) Hamed Amani et al. Journal of Materials Chemistry B
- Circular RNAs Are the Predominant Transcript Isoform from Hundreds of Human Genes in Diverse Cell Types
- (2012) Julia Salzman et al. PLoS One
- Cell Death in the Pathogenesis of Heart Disease: Mechanisms and Significance
- (2010) Russell S. Whelan et al. Annual Review of Physiology
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