SNTA1-deficient human cardiomyocytes demonstrate hypertrophic phenotype and calcium handling disorder

Dong, Tao; Zhao, Yan; Jin, Haifeng; Shen, Lei; Lin, Yan; Si, Longlong; Chen, Li; Liu, Jicheng

doi:10.1186/s13287-022-02955-4

Cited by 2 publications

(2 citation statements)

References 65 publications

(76 reference statements)

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“…STAT1 [435], TLR4 [436], ABCA1 [437], PTGS2 [68], CYP2D6 [438], CR1 [439], PDK4 [440], RNF213 [441], ZDHHC17 [70], TLR8 [442], PDGFC (platelet derived growth factor C) [443], TLR2 [444], CYP1B1 [445], HDAC9 [446], IL1RN [447], GCH1 [448], EGR1 [449], ZEB2 [450], PLA2G7 [451], CCR2 [452], GCLC (glutamate-cysteine ligase catalytic subunit) [258], VEGFA (vascular endothelial growth factor A) [453], CD46 [454], NFKBIZ (NFKB inhibitor zeta) [455], LDLR (low density lipoprotein receptor) [456], TLR6 [457], SIRT1 [458], NOD2 [459], FGL2 [460], IDH1 [461], TET2 [462], PFKFB2 [463], KDM6A [464], IKZF2 [465], ZNF606 [466], PF4 [467], CCR7 [468], RUNX3 [469], TCF7 [470], PPBP (pro-platelet basic protein) [471], IGFBP4 [280], HSPG2 [472] and LGALS3 [236] expression might be regarded as an indicator of susceptibility to CAD. STAT1 [473], TLR4 [367], JAK2 [474], PDGFC (platelet derived growth factor C) [143], CYP1B1 [475], HDAC9 [476], ZEB2 [477], GAB1 [478], IRF9 [479], PHLPP1 [480], SIRT1 [481], NOD2 [482], JMJD1C [483], CLK4 [484], CAVIN1 [485], VEGFB (vascular endothelial growth factor B [486], PRDX2 [487], MAF1 [488], TCF7 [489], IGFBP4 [490], TRPM4 [491], NAA10 [174] and SNTA1 [492] had been demonstrated to participate in cardiac hypertrophy. STAT1 [493], JAK2 [494], NOTCH2 [495], PDGFC (platelet derived growth factor C) [143], RASA1 [262], TLR6 [496...…”

Section: Discussionmentioning

confidence: 99%

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Vastrad¹,

Vastrad²

2023

Preprint

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Coronary artery disease (CAD) is the most common cardiovascular disorder and the leading cause of heart related deaths in world. Increasing molecular targets have been discovered for CAD and CAD - related complications prognosis and therapy. However, there is still an urgent need to identify novel biomarkers. Therefore, we evaluated biomarkers that might help the diagnosis and treatment of CAD and CAD related complications. We searched next generation sequencing (NGS) dataset (GSE202625) and identified differentially expressed genes (DEGs) by comparing CAD and normal control samples using DESeq2. Gene ontology (GO) and pathway enrichment analyses of the DEGs were performed using the g:Profiler online database. The protein protein interaction (PPI) network was plotted with IMEx interactome and visualized using Cytoscape. Module analysis of the PPI network was done using PEWCC1. MiRNA hub gene regulatory network and TF hub gene regulatory network analysis was performed to identify the hub genes, miRNAs and TFs. Receiver operating characteristic (ROC) curve analysis was used to predict the diagnostic effectiveness of the hub genes. A total of 118 DEGs (479 up regulated genes and 479 down regulated genes) were detected. The GO enrichment analysis indicated that the DEGs most significantly enriched in cellular response to stimulus and biosynthetic process. The REACTOME pathway enrichment analysis revealed that the DEGs were most significantly enriched in immune system and eukaryotic translation elongation. PPI network, modules, miRNA hub gene regulatory network and TF hub gene regulatory network analysis demonstrated that EGR1, SIRT1, STAT1, LRRK2, HIF1A, CSNK2B, RPS3, RPS2, RPS4X and HDAC11 were the hub genes. On the whole, the findings of this study enhance our understanding of the potential molecular mechanisms of CAD and CAD-related complications, and provide potential targets for further research.

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Section: Discussionmentioning

confidence: 99%

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Vastrad¹,

Vastrad²

2023

Preprint

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“…The activated SNS will induce the release of neuropeptide Y, which is responsible for the formation of neointima, vasoconstriction and impairment of the immune system [ 80 ]. SNS activation has multiple direct negative effects on the heart, including increasing myocardial oxygen demand, destroying calcium homeostasis, promoting cardiomyocyte apoptosis and hypertrophy [ 81 , 82 , 83 ]. In addition, SNS can further activate RAAS.…”

Section: Molecular Mechanisms Of Crs3mentioning

confidence: 99%

The Molecular Mechanism and Therapeutic Strategy of Cardiorenal Syndrome Type 3

Liu¹,

Xu²,

Shao³

et al. 2023

Rev. Cardiovasc. Med.

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Cardiorenal syndrome type 3 (CRS3) is defined as acute kidney injury (AKI)-induced acute cardiac dysfunction, characterized by high morbidity and mortality. CRS3 often occurs in elderly patients with AKI who need intensive care. Approximately 70% of AKI patients develop into CRS3. CRS3 may also progress towards chronic kidney disease (CKD) and chronic cardiovascular disease (CVD). However, there is currently no effective treatment. Although the major intermediate factors that can mediate cardiac dysfunction remain elusive, recent studies have summarized the AKI biomarkers, identified direct mechanisms, including mitochondrial dysfunction, inflammation, oxidative stress, apoptosis and activation of the sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS), inflammasome, as well as indirect mechanisms such as fluid overload, electrolyte imbalances, acidemia and uremic toxins, which are involved in the pathophysiological changes of CRS3. This study reviews the main pathological characteristics, underlying molecular mechanisms, and potential therapeutic strategies of CRS3. Mitochondrial dysfunction and inflammatory factors have been identified as the key initiators and abnormal links between the impaired heart and kidney, which contribute to the formation of a vicious circle, ultimately accelerating the progression of CRS3. Therefore, targeting mitochondrial dysfunction, antioxidants, Klotho, melatonin, gene therapy, stem cells, exosomes, nanodrugs, intestinal microbiota and Traditional Chinese Medicine may serve as promising therapeutic approaches against CRS3.

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SNTA1-deficient human cardiomyocytes demonstrate hypertrophic phenotype and calcium handling disorder

Cited by 2 publications

References 65 publications

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

Identification of novel prognostic targets in coronary artery disease and related complications using bioinformatics and next generation sequencing data analysis

The Molecular Mechanism and Therapeutic Strategy of Cardiorenal Syndrome Type 3

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