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

The role of m6A RNA methylation in infectious diseases DOI Creative Commons

Nidhi Yadav,

Rafi Ahmad Khan,

Sandeep Goyal

и другие.

Frontiers in RNA Research, Год журнала: 2025, Номер 3

Опубликована: Апрель 10, 2025

Among over 170 known RNA modifications, N 6 -methyladenosine (m A) stands out as the most ubiquitous and extensively studied modification, found in different cellular RNA. The m A plays a pivotal role regulating nuclear export, stability, secondary structure, translation, degradation eventually determining gene expression. modification is controlled by three classes of enzymes: “writers”, “erasers”, “readers” which not only play adding removing methyl group but also help recognizing interpreting methylation marks. Although has been widely context metabolic diseases cancers, its influence on infectious remains under-explored. infection cycle several pathogens, including viruses, bacteria, parasites regulated machinery. In this review, we will explore existing knowledge about shaping pathogen life paving our way to therapeutic aspects mitigate diseases.

Язык: Английский

Процитировано

0

Crosstalk among N6-methyladenosine modification and RNAs in central nervous system injuries DOI Creative Commons
Mi Tian,

Lei Mao,

Li Zhang

и другие.

Frontiers in Cellular Neuroscience, Год журнала: 2022, Номер 16

Опубликована: Сен. 29, 2022

Central nervous system (CNS) injuries, including traumatic brain injury (TBI), intracerebral hemorrhage (ICH) and ischemic stroke, are the most common cause of death disability around world. As modification on ribonucleic acids (RNAs), N6-methyladenosine (m6A) has recently attracted great attentions due to its functions in determining fate RNAs through changes splicing, translation, degradation stability. A large number studies have suggested that m6A played an important role development involved many neurological disorders, particularly CNS injuries. It been proposed could improve impairment, inhibit apoptosis, suppress inflammation, reduce pyroptosis attenuate ferroptosis injuries via different molecules phosphatase tensin homolog (PTEN), NLR family pyrin domain containing 3 (NLRP3), B-cell lymphoma 2 (Bcl-2), glutathione peroxidase 4 (GPX4), long non-coding RNA (lncRNA). Therefore, showed promise as potential targets In this article, we present a review highlighting Hence, basis these properties effects, may be developed therapeutic agents for patients.

Язык: Английский

Процитировано

16

m6A eraser ALKBH5 mitigates the apoptosis of cardiomyocytes in ischemia reperfusion injury through m6A/SIRT1 axis DOI Creative Commons
Liangliang Liu, Zhen Liu

PeerJ, Год журнала: 2023, Номер 11, С. e15269 - e15269

Опубликована: Май 11, 2023

Recent studies have shown that the potential regulatory role of N6-methyladenine (m6A) modification may affect occurrence and development various cardiovascular diseases. However, mechanism m6A on myocardial ischemia reperfusion injury (MIRI) is rarely reported. A mouse model (I/R) was established by ligation perfusion left anterior descending coronary artery, a cellular hypoxia/reperfusion (H/R) conducted in cardiomyocytes (CMs). We found protein expression ALKBH5 tissues cells were decreased, accompanied increased level. Overexpression significantly inhibited H/R-induced oxidative stress apoptosis CMs. Mechanistically, there an enriched motif 3'-UTR SIRT1 genome, overexpression promoted stability mRNA. Furthermore, results using or knockdown confirmed protective effect H/R induced CMs apoptosis. Together, our study reveals critical ALKBH5-medicated CM apoptosis, supplying important regulating methylation ischemic heart disease.

Язык: Английский

Процитировано

9

M6A modification promotes blood-brain barrier breakdown during cerebral ischemia/reperfusion injury through increasing matrix metalloproteinase 3 expression DOI Creative Commons

En Liang,

Shaorong Xiao,

Changtong Zhao

и другие.

Heliyon, Год журнала: 2023, Номер 9(6), С. e16905 - e16905

Опубликована: Июнь 1, 2023

Blood-brain barrier (BBB) breakdown is a critical event in cerebral ischemia-reperfusion (I/R) injury, and matrix metalloproteinases (MMPs), which are proteolytic enzymes, play essential roles BBB through degrading the extracellular matrix. N6-Methyladenosine (m6A), most common reversible mRNA modification, has an important role progression of I/R injury. However, whether m6A related to MMPs expression injury still not clear. In this study, we explored potential effects modification on its underlying mechanisms using mice subjected transient middle artery occlusion reperfusion (MCAO/R), mouse brain endothelial cells treated with oxygen-glucose deprivation reoxygenation (OGD/R). We find that MMP3 highly expressed positively associated writer CBLL1 (Cbl proto-oncogene like 1) vivo vitro. Furthermore, occurs cells, level significantly increased Moreover, inhibition reduces ameliorates conclusion, promotes increasing expression, indicating may be therapeutic target for

Язык: Английский

Процитировано

9

RNA methylation: A potential therapeutic target in autoimmune disease DOI
Lele Li, Xiaoping Xia, Tian Yang

и другие.

International Reviews of Immunology, Год журнала: 2023, Номер 43(3), С. 160 - 177

Опубликована: Ноя. 17, 2023

Autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and inflammatory bowel disease (IBD) are caused by the body's immune response to autoantigens. The pathogenesis of autoimmune is unclear. Numerous studies have demonstrated that RNA methylation plays a key role in progression, which essential for post-transcriptional regulation has gradually become broad regulatory mechanism controls gene expression various physiological processes, including nuclear output, translation, splicing, noncoding processing. Here, we outline writers, erasers, readers methylation, N6-methyladenosine (m6A), 2'-O-methylation (Nm), 2′-O-dimethyladenosine (m6Am), N1-methyladenosine (m1A), 5-methylcytidine (m5C) N7-methylguanosine (m7G). As modifications system explained, potential treatment value these also been demonstrated. This review reports relationship between diseases, highlighting need future research into therapeutic modifications.

Язык: Английский

Процитировано

9

M6A-related bioinformatics analysis indicates that LRPPRC is an immune marker for ischemic stroke DOI Creative Commons

Lianwei Shen,

Shouwei Yue

Scientific Reports, Год журнала: 2024, Номер 14(1)

Опубликована: Апрель 17, 2024

Abstract Ischemic stroke (IS) is a common cerebrovascular disease whose pathogenesis involves variety of immune molecules, channels and processes. 6-methyladenosine (m6A) modification regulates metabolic immunopathological processes, but the role m6A in IS not yet understood. We downloaded data set GSE58294 from GEO database screened for m6A-regulated differential expression genes. The RF algorithm was selected to screen key regulatory Clinical prediction models were constructed validated based on patients grouped according genes, markers identified infiltration characteristics correlation. Finally, we performed functional enrichment, protein interaction network analysis molecular biomarkers. total 7 differentially expressed genes dataset, namely METTL3, WTAP, YWHAG, TRA2A, YTHDF3, LRPPRC HNRNPA2B1. random forest indicated that all IS, credibility above verified by constructing clinical model. Based divided into 2 groups. gene correlation under different subgroups, as an biomarker IS. GO enrichment analyses indicate associated with cellular functions. Protein correlates proteins, may serve target drug therapy. Our findings suggest marker Further could elucidate its microenvironment

Язык: Английский

Процитировано

3

Silencing of YTHDF1 Attenuates Cerebral Stroke by Inducing PTEN Degradation and Activating the PTEN/AKT/mTOR Pathway DOI
Xiaohong Li, Peng An, Fang Han

и другие.

Molecular Biotechnology, Год журнала: 2022, Номер 65(5), С. 822 - 832

Опубликована: Окт. 19, 2022

Язык: Английский

Процитировано

14

RNA methylation reading protein YTHDF2 relieves myocardial ischemia–reperfusion injury by downregulating BNIP3 via m6A modification DOI
Xinyong Cai,

Pengtao Zou,

Lang Hong

и другие.

Human Cell, Год журнала: 2023, Номер 36(6), С. 1948 - 1964

Опубликована: Июль 28, 2023

Язык: Английский

Процитировано

8

RNA methylations in depression, from pathological mechanism to therapeutic potential DOI Open Access
Chen Li,

Pengfei Xu,

Yurong Huang

и другие.

Biochemical Pharmacology, Год журнала: 2023, Номер 215, С. 115750 - 115750

Опубликована: Авг. 16, 2023

Язык: Английский

Процитировано

8

N6-Methyladenosine Methylation of mRNA in Cell Apoptosis DOI
Lin Zhang, Jian Xia

Molecular Neurobiology, Год журнала: 2023, Номер 61(7), С. 3934 - 3948

Опубликована: Дек. 2, 2023

Язык: Английский

Процитировано

6