An overview of the effects and mechanisms of m6 A methylation on innate immune cells in sepsis DOI Creative Commons
Weiwei Qian, Yu Cao

Frontiers in Immunology, Год журнала: 2022, Номер 13

Опубликована: Ноя. 24, 2022

Sepsis is a severe clinical syndrome caused by dysregulated systemic inflammatory responses to infection. Methylation modification, as crucial mechanism of RNA functional can manipulate the immunophenotype and activity immune cells participate in sepsis progression. This study aims explore N6-methyladenosine (m6A) methylation modification cell-mediated through keyword search.Literature retrieval.Literature retrieval reveals that m6A implicated sepsis-induced lung injury myocardial injury,as well sepsis-related encephalopathy. Furthermore, it found regulate inhibiting chemotaxis neutrophils formation neutrophil extracellular traps suppressing macrophage phagocytosis, thereby playing role sepsis.

Язык: Английский

N6-methyladenosine-mediated gene regulation and therapeutic implications DOI
Yujiao Liu, Dan Yang, Tao Liu

и другие.

Trends in Molecular Medicine, Год журнала: 2023, Номер 29(6), С. 454 - 467

Опубликована: Апрель 15, 2023

Язык: Английский

Процитировано

60
Identification of GLS as a cuproptosis-related diagnosis gene in acute myocardial infarction DOI Creative Commons
Zheng Liu, Lei Wang, Qichang Xing

и другие.

Frontiers in Cardiovascular Medicine, Год журнала: 2022, Номер 9

Опубликована: Ноя. 11, 2022

Acute myocardial infarction (AMI) has the characteristics of sudden onset, rapid progression, poor prognosis, and so on. Therefore, it is urgent to identify diagnostic prognostic biomarkers for it. Cuproptosis a new form mitochondrial respiratory-dependent cell death. However, studies are limited on clinical significance cuproptosis-related genes (CRGs) in AMI. In this study, we systematically assessed genetic alterations CRGs AMI by bioinformatics approach. The results showed that six (LIAS, LIPT1, DLAT, PDHB, MTF1, GLS) were markedly differentially expressed between stable coronary heart disease (stable_CAD) Correlation analysis indicated closely correlated with N6-methyladenosine (m6A)-related through R language "corrplot" package, especially GLS was positively FMR1 MTF1 negatively HNRNPA2B1. Immune landscape revealed related various immune cells, T cells CD4 memory resting monocytes. Kaplan-Meier demonstrated group high DLAT expression had better prognosis. area under curve (AUC) certified good value, training set (AUC = 0.87) verification (ACU 0.99). Gene enrichment (GSEA) suggested associated immune- hypoxia-related pathways. addition, Ontology (GO) analysis, Kyoto Encyclopedia Genes Genomes (KEGG) competing endogenous RNA (ceRNA) transcription factor (TF), compound prediction performed reveal regulatory mechanism Overall, our study can provide additional information understanding role AMI, which may insights into identification therapeutic targets

Язык: Английский

Процитировано

45
Regulatory roles of N6-methyladenosine (m6A) methylation in RNA processing and non-communicable diseases DOI
Faiz Ali Khan, Bernard Nsengimana, Usman Ayub Awan

и другие.

Cancer Gene Therapy, Год журнала: 2024, Номер unknown

Опубликована: Июнь 5, 2024

Язык: Английский

Процитировано

9
RNA modification m 6 Am: the role in cardiac biology DOI Creative Commons

Daniel Benák,

František Kolář, Lu Zhang

и другие.

Epigenetics, Год журнала: 2023, Номер 18(1)

Опубликована: Июнь 18, 2023

Epitranscriptomic modifications have recently emerged into the spotlight of researchers due to their vast regulatory effects on gene expression and thereby cellular physiology pathophysiology. N6,2'-O-dimethyladenosine (m6Am) is one most prevalent chemical marks RNA dynamically regulated by writers (PCIF1, METTL4) erasers (FTO). The presence or absence m6Am in affects mRNA stability, regulates transcription, modulates pre-mRNA splicing. Nevertheless, its functions heart are poorly known. This review summarizes current knowledge gaps about modification regulators cardiac biology. It also points out technical challenges lists currently available techniques measure m6Am. A better understanding epitranscriptomic needed improve our molecular regulations which may lead novel cardioprotective strategies.

Язык: Английский

Процитировано

16
Role of m6A RNA Methylation in Ischemic Stroke DOI
Yayun Xu, Wenqiang Liu, Lijie Ren

и другие.

Molecular Neurobiology, Год журнала: 2024, Номер 61(9), С. 6997 - 7008

Опубликована: Фев. 16, 2024

Язык: Английский

Процитировано

6
N6-methyladenosine methylation mediates non-coding RNAs modification in microplastic-induced cardiac injury DOI Creative Commons

Min Zhang,

Jun Shi, Jun Zhou

и другие.

Ecotoxicology and Environmental Safety, Год журнала: 2023, Номер 262, С. 115174 - 115174

Опубликована: Июнь 22, 2023

Owing to their potential adverse health effects, global contamination by microplastics (MPs) has attracted increased scientific and societal concerns. However, in vivo studies on MP toxicity, along with its effects underlying mechanisms, remain limited. We recently found that non-coding RNA (ncRNAs) contribute MP-mediated vascular toxicity. Moreover, previous have identified N6-methyladenosine (m6A) modifications ncRNAs as influencing factors cardiovascular disease. whether how m6A are affected MP-induced cardiotoxicity unknown. Herein, we profiled differentially expressed related modification profiles MP-exposed myocardial tissue using sequencing (RNA-seq) methylated immunoprecipitation (MeRIP-seq). First, observed MPs accumulated different organs upregulated apoptosis the heart, liver, spleen, kidney cells. Furthermore, total METTL3 levels myocardium after exposure MPs. RNA-seq results revealed 392 lncRNAs 302 circRNAs were MP-treated mouse compared control group. Gene Ontology Kyoto Encyclopedia of Genes Genomes enrichment analyses showed these altered closely associated endocytosis, cellular senescence, cell cycle signaling pathways, which may cause cardiotoxicity. MeRIP-seq data distributions abundances circRNAs. Additionally, through conjoint analysis two high-throughput datasets both expression circ-Arfgef2 lncG3bp2 This suggests involved Our findings a better understanding new molecular targets for treating cardiac injury.

Язык: Английский

Процитировано

13
RNA-Binding Proteins as Critical Post-Transcriptional Regulators of Cardiac Regeneration DOI Open Access

De‐Li Shi

International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(15), С. 12004 - 12004

Опубликована: Июль 26, 2023

Myocardial injury causes death to cardiomyocytes and leads heart failure. The adult mammalian has very limited regenerative capacity. However, the from early postnatal mammals lower vertebrates can fully regenerate after apical resection or myocardial infarction. Thus, it is of particular interest decipher mechanism underlying cardiac regeneration that preserves structure function. RNA-binding proteins, as key regulators post-transcriptional gene expression coordinate cell differentiation maintain tissue homeostasis, display dynamic in fetal hearts. Accumulating evidence demonstrated their importance for survival proliferation following neonatal injury. Functional studies suggest proteins relay damage-stimulated extrinsic intrinsic signals regulate capacity by reprogramming multiple molecular cellular processes, such global protein synthesis, metabolic changes, hypertrophic growth, plasticity. Since manipulating activity improve formation new extend window mammals, they are potential targets therapeutic interventions cardiovascular disease. This review discusses our evolving understanding regulating repair regeneration, with aim identify important open questions merit further investigations.

Язык: Английский

Процитировано

12
Klf6 aggravates myocardial ischemia/reperfusion injury by activating Acsl4‐mediated ferroptosis DOI Creative Commons

Mali Qiu,

Wei Yan,

M. Liu

и другие.

The Kaohsiung Journal of Medical Sciences, Год журнала: 2023, Номер 39(10), С. 989 - 1001

Опубликована: Авг. 2, 2023

Abstract Ferroptosis is closely related to myocardial ischemia/reperfusion (I/R) damage. Kruppel‐like factor 6 (Klf6) can aggravate renal I/R injury. We aimed elucidate the role of Klf6 in damage as well its potential mechanism. Myocardial mice model and hypoxia/reoxygenation (H/R)‐treated HL‐1 cells were established. The levels Fe 2+ , MDA, lipid ROS, ferroptosis‐related proteins measured for assessing ferroptosis. Infarct area, H&E staining, cardiac function, cell viability detected evaluating Immunohistochemistry, immunofluorescence, western blot, RT‐qPCR applied detecting genes. m6A modification Klf6, relationships between Mettl3, Igf2bp2, or Acsl4 promoter, was evaluated using MeRIP, RNA immunoprecipitation, pull‐down, chromatin luciferase reporter assay accordingly.Klf6 protein mRNA levels, modification, elevated subjected H/R heart tissues from mice. In H/R‐challenged cells, binding Igf2bp2 Mettl3 confirmed; moreover, knockdown decreased level inhibited stability. restrained H/R‐triggered loss, improved I/R‐induced injury, ferroptosis models. directly bound promoter positively regulated expression. overexpression compromised knockdown‐generated protective effect cells.m6A modification‐regulated aggravated through activating Acsl4‐mediated ferroptosis, thereby providing one target treatment I/R.

Язык: Английский

Процитировано

12
Deepm6A-MT: A deep learning-based method for identifying RNA N6-methyladenosine sites in multiple tissues DOI
Guohua Huang,

Xiaohong Huang,

Jinyun Jiang

и другие.

Methods, Год журнала: 2024, Номер 226, С. 1 - 8

Опубликована: Март 12, 2024

Язык: Английский

Процитировано

4
Insights From m6A RNA Methylation: Biomarkers for Diagnosis of Acute Myocardial Infarction DOI Creative Commons
Wenjun Fan, Wenbin Zhao,

Renjie Hu

и другие.

Journal of Inflammation Research, Год журнала: 2025, Номер Volume 18, С. 3589 - 3605

Опубликована: Март 1, 2025

Purpose: Acute myocardial infarction (AMI) is a major contributor to death. The purpose of this study explore circulating biomarkers for AMI diagnosis from the perspectives immunological microenvironment and N6-methyladenosine (m6A) RNA methylation regulation. Patients Methods: GSE59867 dataset was used download platform probe data conducting differential analysis m6A regulators. A diagnostic nomogram created utilizing random-forest method evaluated predictive power. m6A-related gene patterns were identified, their immune characteristics analyzed. Peripheral blood samples obtained validation in patient-based investigations using RT-qPCR. association between regulators clinical parameters examined via Spearman correlation analysis. Results: With model developed key regulators, two distinct subtypes showing significant variations infiltrating immunocyte abundance. In confirmation prediction, examination patient identified METTL3, WTAP, RBM15, ALKBH5, FTO, FMR1 as novel diagnosis. METTL3 FTO promising given that they showed positive with left ventricular ejection fraction. Conclusion: six suggested potential role m6A-mediated cell infiltration pathogenesis AMI. Keywords: acute infarction, infiltration, N6-methyladenosine, diagnosis, biomarker

Язык: Английский

Процитировано

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