Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis DOI Open Access
Basavaraj Vastrad, Chanabasayya Vastrad

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: June 25, 2024

Huntington's disease (HD) is the primary cause of progressive motor deficits, psychiatric symptoms, and cognitive impairment. The exact molecular mechanisms HD pathogenesis are largely unknown. This investigation aims to identify hub genes, miRNA TFs in explore their potential regulatory network. Next generation sequencing (NGS) dataset (GSE105041) was extracted from Gene Expression Omnibus (GEO) database. An integrated bioinformatics pipeline including identification differentially expressed genes (DEGs), ontology REACTOME pathway enrichment analysis, protein-protein interaction (PPI) network module miRNA-hub gene analysis TF-hub receiver operating characteristic curve (ROC) were applied TFs, key drivers pathogenesis. We identified 958 DEGs discovery phase, consisting 479 up regulated down genes. GO analyses showed that they mainly involved multicellular organismal process, developmental signaling by GPCR MHC class II antigen presentation. Further PPI using Cytoscape PEWCC plugins 10 LRRK2, MTUS2, HOXA1, IL7R, ERBB3, EGFR, TEX101, WDR76, NEDD4L COMT. Possible target miRNAs hsa-mir-1292-5p, hsa-mir-4521, ESRRB SREBF1, predicted constructing a used methods HD, markers. These markers might provide novel ideas for early diagnosis, treatment, monitoring HD.

Language: Английский

Maresin‐1 ameliorates hypertensive vascular remodeling through its receptor LGR6 DOI Creative Commons
Zheng Yin, Jishou Zhang, Mengmeng Zhao

et al.

MedComm, Journal Year: 2024, Volume and Issue: 5(3)

Published: March 1, 2024

Abstract Hypertensive vascular remodeling is defined as the changes in function and structure induced by persistent hypertension. Maresin‐1 (MaR1), one of metabolites from Omega‐3 fatty acids, has been reported to promote inflammation resolution several inflammatory diseases. This study aims investigate effect MaR1 on hypertensive remodeling. Here, we found serum levels were reduced patients was negatively correlated with systolic blood pressure (SBP). The treatment elevation alleviated angiotensin II (AngII)‐infused mouse model. In addition, MaR1‐treated smooth muscle cells (VSMCs) exhibited excessive proliferation, migration, phenotype switching, well impaired pyroptosis. However, knockout receptor MaR1, leucine‐rich repeat‐containing G protein‐coupled 6 (LGR6), seen aggravate pathological remodeling, which could not be reversed additional treatment. mechanisms regulates through LGR6 involves Ca 2+ /calmodulin‐dependent protein kinase II/nuclear factor erythroid 2‐related 2/heme oxygenase‐1 signaling pathway. Overall, supplementing may a novel therapeutic strategy for prevention

Language: Английский

Citations

10
EDIL3/Del-1 prevents aortic dissection through enhancing internalization and degradation of apoptotic vascular smooth muscle cells DOI
Zheng Yin, Jishou Zhang, Mengmeng Zhao

et al.

Autophagy, Journal Year: 2024, Volume and Issue: unknown, P. 1 - 21

Published: June 14, 2024

Thoracic aortic dissection (TAD) is a severe disease, characterized by numerous apoptotic vascular smooth muscle cells (VSMCs). EDIL3/Del-1 secreted protein involved in macrophage efferocytosis acute inflammation. Here, we aimed to investigate whether EDIL3 promoted the internalization and degradation of VSMCs during TAD. The levels were decreased serum tissue from TAD mice. Global

Language: Английский

Citations

7
Resolution of inflammation, an active process to restore the immune microenvironment balance: A novel drug target for treating arterial hypertension DOI
Jishou Zhang, Siqi Liu, Wen Ding

et al.

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 99, P. 102352 - 102352

Published: June 9, 2024

Language: Английский

Citations

6
Regulated vascular smooth muscle cell death in vascular diseases DOI Creative Commons
Zheng Yin,

Jishou Zhang,

Zican Shen

et al.

Cell Proliferation, Journal Year: 2024, Volume and Issue: unknown

Published: June 14, 2024

Abstract Regulated cell death (RCD) is a complex process that involves several types and plays crucial role in vascular diseases. Vascular smooth muscle cells (VSMCs) are the predominant elements of medial layer blood vessels, their regulated contributes to pathogenesis The VSMC include apoptosis, necroptosis, pyroptosis, ferroptosis, parthanatos, autophagy‐dependent (ADCD). In this review, we summarize current evidence pathways major diseases, such as atherosclerosis, calcification, aortic aneurysm dissection, hypertension, pulmonary arterial neointimal hyperplasia, inherited All forms RCD constitute single, coordinated system which one pathway can compensate for another during disease progression. Pharmacologically targeting has potential slowing reversing progression, but challenges remain. A better understanding diseases underlying mechanisms may lead novel pharmacological developments help clinicians address residual cardiovascular risk patients with

Language: Английский

Citations

6
Plant-Derived Nanovesicles as Novel Nanotherapeutics for Alleviating Endothelial Cell Senescence-Associated Vascular Remodeling Induced by Hypertension DOI Creative Commons

Fengxia Lin,

Luhua Xu,

Qin He

et al.

Pharmacological Research, Journal Year: 2025, Volume and Issue: 214, P. 107675 - 107675

Published: Feb. 25, 2025

Language: Английский

Citations

0
Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis DOI Creative Commons
Basavaraj Vastrad, Chanabasayya Vastrad

Egyptian Journal of Medical Human Genetics, Journal Year: 2025, Volume and Issue: 26(1)

Published: March 4, 2025

Abstract Background Huntington's disease (HD) could cause progressive motor deficits, psychiatric symptoms, and cognitive impairment. With the increasing use of pharmacotherapies theoretically target neurotransmitters, incidence HD is still not decreasing. However, molecular pathogenesis have been illuminate. It momentous to further examine HD. Methods The next generation sequencing dataset GSE105041 was downloaded from Gene Expression Omnibus (GEO) database. Using DESeq2 in R bioconductor package screen differentially expressed genes (DEGs) between samples normal control samples. ontology (GO) term REACTOME pathway enrichment were performed on DEGs. Meanwhile, using Integrated Interactions Database (IID) database Cytoscape software construct protein–protein interaction (PPI) network module analysis, identify hub with highest value node degree, betweenness, stress closeness scores. miRNA-hub gene regulatory TF-hub constructed analyzed. Receiver operating characteristic curves analysis for diagnostic genes. Results We identified 958 DEGs, consisting 479 up regulated DEGs down GO terms analyses by g:Profiler online results revealed that mainly enriched multicellular organismal process, developmental signaling GPCR MHC class II antigen presentation. Network Analyzer plugin PPI network, LRRK2, MTUS2, HOXA1, IL7R, ERBB3, EGFR, TEX101, WDR76, NEDD4L COMT selected as Hsa-mir-1292-5p, hsa-mir-4521, ESRRB SREBF1 are potential biomarkers predicted be associated Conclusion This study investigated key pathways interactions its complications, which might help reveal correlation complications. current investigation captured prediction, follow-up biological experiments enforced validation.

Language: Английский

Citations

0
Leucine‐Rich Repeat‐Containing G Protein‐Coupled Receptor 6 Ameliorates Pressure Overload‐Induced Cardiac Hypertrophy by Regulating Cardiomyocyte Metabolic Reprogramming DOI Creative Commons
Mengmeng Zhao, Jianfang Liu, Shanshan Peng

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: April 11, 2025

Abstract Metabolic reprogramming is a pivotal mechanism in the pathogenesis of pathological cardiac hypertrophy. Leucine‐rich repeat‐containing G protein‐coupled receptor 6 (Lgr6) has emerged as significant player cardiovascular diseases. In this study, potential Lgr6 to counteract pressure overload (PO)‐induced hypertrophy investigated, and underlying mechanisms involved are elucidated. Transverse aortic constriction (TAC) induced establish an vivo model. Adeno‐associated virus 9 adenovirus vectors utilized knock down overexpress cardiomyocytes, respectively. The effects its downstream molecules subsequently determined using RNA sequencing chromatin immunoprecipitation. Significant downregulation expression observed heart after TAC cardiomyocytes treated with phenylephrine. deficiency accelerated overexpression inhibits dysfunction TAC. Mechanistically, vitro experiments suggest that regulates ubiquitin specific protease 4 (USP4) peroxisome proliferator‐activated alpha (PPARα) by activating cGMP/PKG/CREB1 signalling pathway, thereby regulating cardiomyocyte metabolic PO. Targeting can be therapeutic strategy treat

Language: Английский

Citations

0
Pro-resolving lipid mediators and therapeutic innovations in resolution of inflammation DOI
Hong Yong Peh, Jianmin Chen

Pharmacology & Therapeutics, Journal Year: 2024, Volume and Issue: unknown, P. 108753 - 108753

Published: Nov. 1, 2024

Language: Английский

Citations

3
F-53B stimulated vascular smooth muscle cell phenotypic switch and vascular remodeling via ferroptosis-related pathway DOI
M. Zhang, Jun Shi,

Huichao Pan

et al.

The Science of The Total Environment, Journal Year: 2024, Volume and Issue: 954, P. 176565 - 176565

Published: Sept. 27, 2024

Language: Английский

Citations

2
Identification of key genes and signaling pathway in the pathogenesis of Huntington's disease via bioinformatics and next generation sequencing data analysis DOI Open Access
Basavaraj Vastrad, Chanabasayya Vastrad

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown

Published: June 25, 2024

Huntington's disease (HD) is the primary cause of progressive motor deficits, psychiatric symptoms, and cognitive impairment. The exact molecular mechanisms HD pathogenesis are largely unknown. This investigation aims to identify hub genes, miRNA TFs in explore their potential regulatory network. Next generation sequencing (NGS) dataset (GSE105041) was extracted from Gene Expression Omnibus (GEO) database. An integrated bioinformatics pipeline including identification differentially expressed genes (DEGs), ontology REACTOME pathway enrichment analysis, protein-protein interaction (PPI) network module miRNA-hub gene analysis TF-hub receiver operating characteristic curve (ROC) were applied TFs, key drivers pathogenesis. We identified 958 DEGs discovery phase, consisting 479 up regulated down genes. GO analyses showed that they mainly involved multicellular organismal process, developmental signaling by GPCR MHC class II antigen presentation. Further PPI using Cytoscape PEWCC plugins 10 LRRK2, MTUS2, HOXA1, IL7R, ERBB3, EGFR, TEX101, WDR76, NEDD4L COMT. Possible target miRNAs hsa-mir-1292-5p, hsa-mir-4521, ESRRB SREBF1, predicted constructing a used methods HD, markers. These markers might provide novel ideas for early diagnosis, treatment, monitoring HD.

Language: Английский

Citations

0