m<sup>6</sup>A RNA methylation drives kidney fibrosis by upregulating β-catenin signaling

Long, Yinyi; Song, Dongyan; Xiao, Liuyan; Xiang, Yadie; Li, Dier; Sun, Xiaoli; Hong, Xue; Hou, Fan Fan; Fu, Haiyan; Liu, Youhua

doi:10.7150/ijbs.96233

Int. J. Biol. Sci.

2024

DOI: 10.7150/ijbs.96233

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m⁶A RNA methylation drives kidney fibrosis by upregulating β-catenin signaling

Yinyi Long,

Dongyan Song,

Liuyan Xiao

et al.

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Cited by 4 publications

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m6A modification in non-coding RNAs: Mechanisms and potential therapeutic implications in fibrosis

Zhou,

Jian,

Jiang

et al. 2024

Biomedicine & Pharmacotherapy

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m6A modification in non-coding RNAs: Mechanisms and potential therapeutic implications in fibrosis

Zhou,

Jian,

Jiang

et al. 2024

Biomedicine & Pharmacotherapy

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Kidney Fibrosis: Fundamental Questions, Challenges, and Perspectives

Liu

2024

Integr Med Nephrol Androl

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Methyltransferase-like 3 represents a prospective target for the diagnosis and treatment of kidney diseases

Song,

Wu,

Zeng

2024

Hum Genomics

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Kidney disease is marked by complex pathological mechanisms and significant therapeutic hurdles, resulting in high morbidity and mortality rates globally. A deeper understanding of the fundamental processes involved can aid in identifying novel therapeutic targets and improving treatment efficacy. Current comprehensive data analyses indicate the involvement of methyltransferase-like 3 (METTL3) and its role in RNA N 6 -methyladenosine methylation in various renal pathologies, including acute kidney injury, renal fibrosis, and chronic kidney disease. However, there is a paucity of thorough reviews that clarify the functional mechanisms of METTL3 and evaluate its importance in enhancing therapeutic outcomes. This review seeks to systematically examine the roles, mechanisms, and potential clinical applications of METTL3 in renal diseases. The findings presented suggest that METTL3 is implicated in the etiology and exacerbation of kidney disorders, affecting their onset, progression, malignancy, and responsiveness to chemotherapeutic agents through the regulation of specific genetic pathways. In conclusion, this review underscores a detrimental correlation between METTL3 and kidney diseases, highlighting the therapeutic promise of targeting METTL3. Additionally, it offers critical insights for researchers concerning the diagnosis, prognosis, and treatment strategies for renal conditions.

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m⁶A RNA methylation drives kidney fibrosis by upregulating β-catenin signaling

Cited by 4 publications

References 44 publications

m6A modification in non-coding RNAs: Mechanisms and potential therapeutic implications in fibrosis

m6A modification in non-coding RNAs: Mechanisms and potential therapeutic implications in fibrosis

Kidney Fibrosis: Fundamental Questions, Challenges, and Perspectives

Methyltransferase-like 3 represents a prospective target for the diagnosis and treatment of kidney diseases

Contact Info

Product

Resources

About

m6A RNA methylation drives kidney fibrosis by upregulating β-catenin signaling

Cited by 4 publications

References 44 publications

m6A modification in non-coding RNAs: Mechanisms and potential therapeutic implications in fibrosis

m6A modification in non-coding RNAs: Mechanisms and potential therapeutic implications in fibrosis

Kidney Fibrosis: Fundamental Questions, Challenges, and Perspectives

Methyltransferase-like 3 represents a prospective target for the diagnosis and treatment of kidney diseases

Contact Info

Product

Resources

About

m⁶A RNA methylation drives kidney fibrosis by upregulating β-catenin signaling