STAMP2 Attenuates Cardiac Dysfunction and Insulin Resistance in Diabetic Cardiomyopathy via NMRAL1-Mediated NF-κB Inhibition in Type 2 Diabetic Rats

Gao, Zhan; Ti, Yun; Lü, Bin; Song, Fang-qiang; Zhang, Lei; Hu, Bo-ang; Liu, Juewen; Zhang, Wei; Han, Lu; Zhong, Ming

doi:10.2147/dmso.s374784

Cited by 3 publications

(3 citation statements)

References 25 publications

(27 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies had shown that KCNJ2 [136], ARG1 [137], TLR4 [138], IFIH1 [139], FBN2 [140], PDK4 [141], TLR8 [142], PDGFC (platelet derived growth factor C) [143], FNIP1 [144], TLR2 [145], PTPN11 [146], LATS2 [147], GCH1 [148], ARFGEF2 [149], CA2 [150], PTPRC (protein tyrosine phosphatase receptor type C) [151], CCR2 [152], GAB1 [153], VEGFA (vascular endothelial growth factor A) [154], UBR1 [155], PHLPP1 [156], MTM1 [157], FMR1 [158], SIRT1 [159], NOD2 [160], MYOF (myoferlin) [161], OSBPL11 [162], ZBTB11 [121], UTRN (utrophin) [163], ZNF593 [164], CCR7 [165], PRDX2 [166], BIN1 [167], NFIC (nuclear factor I C) [168], TCF4 [169], PPP1R13L [124], NDUFB11 [170], TAX1BP3 [171], TRPM4 [172], NMRAL1 [173], LGALS3 [126] and NAA10 [174] were associated with cardiomyopathy. CD274 [175], CEACAM1 [176], STAT1 [177], ARG1 [178], TLR4 [179], LRRK2 [180], ABCA1 [181], IFIH1 [182], TLR5 [183], PTGS2 [184], CYP2D6 [185], RNF213 [186], C9ORF72 [187], JAK2 [188], TLR8 [189], NOTCH2 [190], PDGFC (platelet derived growth factor C) [191], TLR2 [192], PRKAB2 [193], HDAC9 [194], NCOA4 [195], LATS2 [196], DICER1 [197], IL1RN [198], GCH1 [148], EGR1 [199], HIPK3 [200], ZEB2 [201], HIF1A [202], PLA2G7 [203], DOCK8 [204], CCR2 [205], PPP1R15B [206], GCLC (...…”

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

View full text Add to dashboard Cite

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.

show abstract

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

View full text Add to dashboard Cite

show abstract

“…114,117 IKK/NF-κB signal pathway was involved in IR in DM. 115,118 In DCM, activating PI3K/AKT signal pathway or inhibiting NF-κB signal pathway could reduce the occurrence of IR, 119,120 and AKT2 deficiency resulted in severe glucose intolerance, myocardial contractile dysfunction, cardiomyocyte apoptosis, and impaired cardiac function. 121,122 IRS1/PI3K/AKT pathway was the main signal regulation pathway of podocyte IR, and blocking this pathway would induce EMT and glomerulosclerosis in DN podocytes.…”

Section: Impaired Insulin Signaling Pathwaysmentioning

confidence: 99%

Inflammation in diabetes complications: molecular mechanisms and therapeutic interventions

Zhao,

Hu,

Zhang

et al. 2024

MedComm

View full text Add to dashboard Cite

At present, diabetes mellitus (DM) has been one of the most endangering healthy diseases. Current therapies contain controlling high blood sugar, reducing risk factors like obesity, hypertension, and so on; however, DM patients inevitably and eventually progress into different types of diabetes complications, resulting in poor quality of life. Unfortunately, the clear etiology and pathogenesis of diabetes complications have not been elucidated owing to intricate whole‐body systems. The immune system was responsible to regulate homeostasis by triggering or resolving inflammatory response, indicating it may be necessary to diabetes complications. In fact, previous studies have been shown inflammation plays multifunctional roles in the pathogenesis of diabetes complications and is attracting attention to be the meaningful therapeutic strategy. To this end, this review systematically concluded the current studies over the relationships of susceptible diabetes complications (e.g., diabetic cardiomyopathy, diabetic retinopathy, diabetic peripheral neuropathy, and diabetic nephropathy) and inflammation, ranging from immune cell response, cytokines interaction to pathomechanism of organ injury. Besides, we also summarized various therapeutic strategies to improve diabetes complications by target inflammation from special remedies to conventional lifestyle changes. This review will offer a panoramic insight into the mechanisms of diabetes complications from an inflammatory perspective and also discuss contemporary clinical interventions.

show abstract

“…Studies, both preclinical and clinical, have shown that DM induces a pro-fibrotic state. Four-week-old male Sprague–Dawley rats with streptozocin-induced DM exhibited a higher collagen type I and III accumulation compared to the control group [ 62 ]. Critically, a recently published systematic review and meta-analysis of 32 studies by Salvador et al highlighted a relationship between DM and a higher degree of myocardial fibrosis assessed by either the histological collagen volume fraction (mean difference 5.80; 95% CI: 2.00–9.59) or extracellular volume fraction (mean difference: 2.09; 95% CI: 0.92–3.27) [ 63 ].…”

Section: The Role Of Diabetes Mellitus In Heart Failure Pathophysiologymentioning

confidence: 99%

Diabetes Mellitus and Heart Failure: Epidemiology, Pathophysiologic Mechanisms, and the Role of SGLT2 Inhibitors

Theofilis

Oikonomou

Tsioufis

et al. 2023

Life

View full text Add to dashboard Cite

Diabetes mellitus (DM) and heart failure (HF) are frequently encountered afflictions that are linked by a common pathophysiologic background. According to landmark studies, those conditions frequently coexist, and this interaction represents a poor prognostic indicator. Based on mechanistic studies, HF can be propagated by multiple pathophysiologic pathways, such as inflammation, oxidative stress, endothelial dysfunction, fibrosis, cardiac autonomic neuropathy, and alterations in substrate utilization. In this regard, DM may augment myocardial inflammation, fibrosis, autonomic dysfunction, and lipotoxicity. As the interaction between DM and HF appears critical, the new cornerstone in DM and HF treatment, sodium-glucose cotransporter-2 inhibitors (SGLT2i), may be able to revert the pathophysiology of those conditions and lead to beneficial HF outcomes. In this review, we aim to highlight the deleterious pathophysiologic interaction between DM and HF, as well as demonstrate the beneficial role of SGLT2i in this field.

show abstract

STAMP2 Attenuates Cardiac Dysfunction and Insulin Resistance in Diabetic Cardiomyopathy via NMRAL1-Mediated NF-κB Inhibition in Type 2 Diabetic Rats

Cited by 3 publications

References 25 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

Inflammation in diabetes complications: molecular mechanisms and therapeutic interventions

Diabetes Mellitus and Heart Failure: Epidemiology, Pathophysiologic Mechanisms, and the Role of SGLT2 Inhibitors

Contact Info

Product

Resources

About