N6-Methyladenosine (m6A) Modification in Natural Immune Cell-Mediated Inflammatory Diseases

Teng, Yan; Yi, Jin; Chen, Junnian; Yang, Lu

doi:10.1159/000534162

Cited by 3 publications

(2 citation statements)

References 109 publications

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“…The activation of inflammatory processes in the brain, involving immune cells such as microglia, astrocytes, and infiltrating blood cells, leads to the release of pro-inflammatory cytokines (118). So far, the development, differentiation, and activation processes of these immune cells have all been shown to be regulated by m6A, thus affecting the inflammatory response process (119).…”

Section: M6a and Neuroinflammationmentioning

confidence: 99%

RNA m6A Methylation and Alzheimer's Disease: Current Evidence and Future Perspectives

Pan,

Chen,

et al. 2024

Human Brain

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Background: Alzheimer’s disease (AD) is the most common neurodegenerative disease characterized by the pathological accumulation of b-amyloid and neurofibrillary tangles. Despite substantial progress in both basic and clinical research on AD, the detailed mechanism of AD pathogenesis is still elusive. RNA N6-methyladenosine methylation (m6A) is the most predominant post-transcriptional modification on eukaryotic mRNA, prominently enriched in the mammalian brain. Notably, m6A-modified RNA showed significant changes during the development of AD, indicating an important role of this modification in AD pathogenesis. Aim: In this study, we aim to provide a summary of recent advances highlighting the indispensable role of m6A in AD pathogenesis. Result: From the perspective of m6A modification, we review our current understanding of the association between RNA m6A machinery and the risk factors of AD, as well as its involvement in various pathophysiological hallmarks of AD. We also discuss the main obstacles in current studies about m6A in AD pathogenesis and the corresponding caveats and solutions to them. Conclusion: This review emphasizes the significance of investigating m6A in the context of AD and highlights the considerable potential for m6A to emerge as a novel therapeutic target for AD.

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Section: M6a and Neuroinflammationmentioning

confidence: 99%

RNA m6A Methylation and Alzheimer's Disease: Current Evidence and Future Perspectives

Pan,

Chen,

et al. 2024

Human Brain

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“…The recognition of such modi cations on RNA by m6A readers can impact RNA stability and essential biological processes, such as transport and translation 10 . m6A modi cation can orchestrate the development, differentiation, and activation of immune cells, consequently affecting the host defense and in ammatory responses to pathogens 11 . Dysregulated m6A modi cations contribute to the pathogenesis of immune-related diseases 12 .…”

Section: Introductionmentioning

confidence: 99%

METTL3 Deficiency Aggravates Hepatic Ischemia/Reperfusion Injury in Mice by Activating the MAPK Signaling Pathway

Gao,

Wang,

Qin

et al. 2024

Preprint

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Inflammatory responses, apoptosis, and oxidative stress, are key factors that contribute to hepatic ischemia/reperfusion (I/R) injury, which may lead to the failure of liver surgeries, such as hepatectomy and liver transplantation. The N6-methyladenosine (m6A) modification has been implicated in multiple biological processes, and its specific role and mechanism in hepatic I/R injury require further investigation. This study focused on the role of RNA methylase METTL3 in hepatic ischemia-reperfusion injury. Dot blotting analysis was used to profile m6A levels in liver tissues at different reperfusion time points in hepatic I/R mouse models. Hepatocyte-specific METTL3 knockdown (HKD) mice were used to determine the function of METTL3 during hepatic I/R. RNA sequencing and western blotting were performed to assess the potential signaling pathways involved with the deficiency of METTL3. Finally, AAV8-TBG-METTL3 was injected through the tail vein to further elucidate the role of METTL3 in hepatic I/R injury. We found that the m6A modification levels and the expression of METTL3 were upregulated in mouse livers during hepatic I/R injury. METTL3 deficiency led to an exacerbated inflammatory response and increased cell death during hepatic I/R, whereas overexpression of METTL3 reduced the extent of liver injury. Bioinformatic analysis revealed that the MAPK pathway was significantly enriched in the livers of METTL3-deficient mice. METTL3 protected the liver from I/R injury, possibly by inhibiting the phosphorylation of JNK and ERK, but not P38.

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The Role of m6A Methylation in Tumor Immunity and Immune-Associated Disorder

Mu,

Zhao,

Zhong

et al. 2024

Biomolecules

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N6-methyladenosine (m6A) represents the most prevalent and significant internal modification in mRNA, with its critical role in gene expression regulation and cell fate determination increasingly recognized in recent research. The immune system, essential for defense against infections and maintaining internal stability through interactions with other bodily systems, is significantly influenced by m6A modification. This modification acts as a key post-transcriptional regulator of immune responses, though its effects on different immune cells vary across diseases. This review delineates the impact of m6A modification across major system-related cancers—including those of the respiratory, digestive, endocrine, nervous, urinary reproductive, musculoskeletal system malignancies, as well as acute myeloid leukemia and autoimmune diseases. We explore the pathogenic roles of m6A RNA modifications within the tumor immune microenvironment and the broader immune system, highlighting how RNA modification regulators interact with immune pathways during disease progression. Furthermore, we discuss how the expression patterns of these regulators can influence disease susceptibility to immunotherapy, facilitating the development of diagnostic and prognostic models and pioneering new therapeutic approaches. Overall, this review emphasizes the challenges and prospective directions of m6A-related immune regulation in various systemic diseases throughout the body.

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N6-Methyladenosine (m6A) Modification in Natural Immune Cell-Mediated Inflammatory Diseases

Cited by 3 publications

References 109 publications

RNA m6A Methylation and Alzheimer's Disease: Current Evidence and Future Perspectives

RNA m6A Methylation and Alzheimer's Disease: Current Evidence and Future Perspectives

METTL3 Deficiency Aggravates Hepatic Ischemia/Reperfusion Injury in Mice by Activating the MAPK Signaling Pathway

The Role of m6A Methylation in Tumor Immunity and Immune-Associated Disorder

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