m6A Ribonucleic Acid Methylation in Fibrotic Diseases of Visceral Organs DOI Creative Commons

Xiaoniu Dai,

Yusi Cheng, Wei Luo

et al.

Small Science, Journal Year: 2024, Volume and Issue: unknown

Published: Nov. 21, 2024

Fibrosis is a pathological process characterized by the excessive deposition of extracellular matrix in tissue's space, leading to structural injury and organ dysfunction, even failure, posing threat human life. Despite mounting evidence suggesting that fibrosis reversible, effective treatments for fibrotic diseases are lacking. Accumulating has elucidated ribonucleic acid (RNA) modifications have emerged as novel mechanisms regulating gene expression. N6‐methyladenosine (m6A) modification well‐known prevalent RNA posttranscriptional participates essential biological processes such splicing, translation, degradation. It tightly implicated wide range cellular various diseases, particularly fibrosis. The m6A dynamic reversible regulated methylases, commonly known “writers,” demethylases referred “erasers,” while recognized “readers.” suggests on RNAs associated with visceral organs including lungs, heart, liver, kidney. In this review, recent advances impact methylation highlighted potential prospects therapy treating discussed.

Language: Английский

The Emerging Role of m6A and Programmed Cell Death in Cardiovascular Diseases DOI Creative Commons
Haixia Wang, Juanjuan Han, Hui Kong

et al.

Biomolecules, Journal Year: 2025, Volume and Issue: 15(2), P. 247 - 247

Published: Feb. 8, 2025

N6-methyladenosine (m6A) is the most prevalent internal chemical modification in eukaryotic messenger RNA (mRNA), significantly impacting its lifecycle through dynamic and reversible processes involving methyltransferase, demethylase, binding proteins. These regulate mRNA stability, splicing, nuclear export, translation, degradation. Programmed cell death (PCD), a tightly controlled process encompassing apoptosis, pyroptosis, ferroptosis, autophagy, necroptosis, plays crucial role maintaining cellular homeostasis, tissue development, function. Recently, m6A has emerged as significant research area due to regulating PCD implications cardiovascular diseases (CVDs). In this review, we delve into intricate relationship between various types modification, emphasizing their pivotal roles initiation progression of CVDs such myocardial ischemia-reperfusion (I/R), atherosclerosis (AS), pulmonary hypertension (PH), cardiomyopathy, doxorubicin (Dox)-induced cardiotoxicity (DIC), heart failure (HF), infarction (MI). Our findings underscore potential elucidating CVD pave new pathways for prevention treatment strategies.

Language: Английский

Citations

2
Programmed Release METTL3-14 Inhibitor Microneedle Protects Myocardial Function by Reducing Drp1 m6A Modification-Mediated Mitochondrial Fission DOI Creative Commons
Boyue Huang,

Xie Liu,

Ke Ming

et al.

ACS Applied Materials & Interfaces, Journal Year: 2023, Volume and Issue: 15(40), P. 46583 - 46597

Published: Sept. 27, 2023

M6A modification is an RNA-important processing event mediated by methyltransferases METTL3 and METTL14 the demethylases. dynamic changes after myocardial infarction (MI), involved in massive loss of cardiomyocytes due to hypoxia, as well recruitment activation myofibroblasts. Balanced mitochondrial fusion fission are essential maintain intracardiac homeostasis reduce poststress remodeling. Double-layer programmed drug release microneedle (DPDMN) breaks limitations existing therapeutic interventions one period or type cells, multitargeted cellular combination has more potential MI therapy. By employing hypoxia-ischemic TGF-β1-induced fibrosis cell models, we found that METTL3-14 inhibition effectively decreased cardiomyocyte death through reduction fragmentation inhibiting myofibrillar transformation. DPDMN treatment rat models showed improved cardiac function infarct size level, demonstrating its superior effectiveness. The delivers inhibitor swiftly early phase rescue dying slowly late achieve long-term suppression fibroblast over proliferation, collagen synthesis, deposition. RIP assay mechanistic investigation confirmed reduced translation efficiency Drp1 mRNA 5′UTR m6A modification, thus decreasing protein level fragment hypoxic-ischemic injury. This project investigated efficacy DPDMNs-loaded downstream signaling pathway proteins, providing experimental foundation for utility, safety, versatility delivery into clinical applications.

Language: Английский

Citations

17
m6A control programmed cell death in cardiac fibrosis DOI
Zhenyu Liu,

Qing-Ye You,

Zhiyan Liu

et al.

Life Sciences, Journal Year: 2024, Volume and Issue: 353, P. 122922 - 122922

Published: July 18, 2024

Language: Английский

Citations

5
N6-methyladenosine (m6A) RNA modification in fibrosis and collagen-related diseases DOI Creative Commons

Man Tan,

Siyi Liu, Lubin Liu

et al.

Clinical Epigenetics, Journal Year: 2024, Volume and Issue: 16(1)

Published: Sept. 12, 2024

Language: Английский

Citations

5
m6A RNA modification pathway: orchestrating fibrotic mechanisms across multiple organs DOI Creative Commons

Xiangfei Huang,

Zilu Yu,

Juan Tian

et al.

Briefings in Functional Genomics, Journal Year: 2025, Volume and Issue: 24

Published: Jan. 1, 2025

Organ fibrosis, a common consequence of chronic tissue injury, presents significant health challenge. Recent research has revealed the regulatory role N6-methyladenosine (m6A) RNA modification in fibrosis various organs, including lung, liver, kidney, and heart. In this comprehensive review, we summarize latest findings on mechanisms functions m6A organ fibrosis. By highlighting potential as therapeutic target, our goal is to encourage further emerging field support advancements clinical treatment

Language: Английский

Citations

0
A comprehensive review of m6 A methylation in coronary heart disease DOI
Mei-Ning Diao, Yingli Lv, Xin Hui

et al.

Journal of Molecular Medicine, Journal Year: 2025, Volume and Issue: unknown

Published: April 10, 2025

Language: Английский

Citations

0
Epigenetic modifications in cardiac fibrosis: recent evidence of new pharmacological targets DOI Creative Commons
M. Sánchez Pérez, Mónica Gómez, Jairo Castellar-López

et al.

Frontiers in Molecular Biosciences, Journal Year: 2025, Volume and Issue: 12

Published: May 2, 2025

Cardiac fibrosis (CF) is characterized by the excessive deposition of collagen types I (COI I) and III III), primarily mediated cardiac fibroblasts (CFB). Recent advances in epigenetic research have enhanced our understanding molecular mechanisms underlying CF facilitated identification novel therapeutic strategies targeting key proteins signaling pathways involved its progression. Epigenetic modifications, including DNA methylation, histone non-coding RNAs (ncRNAs), are structural chemical alterations that regulate gene expression cellular responses without changing sequence. Investigating role enzymes may reveal promising pharmacological targets. This review summarizes current evidence on modifications implicated discusses their potential as targets for modulating this pathological process.

Language: Английский

Citations

0
METTL3-mediated m⁶A methylation in cardiac diseases: pathogenic roles and therapeutic potential DOI Creative Commons
Ruida Liu, Xiaojuan Su, Lei Yang

et al.

Cell Biology and Toxicology, Journal Year: 2025, Volume and Issue: 41(1)

Published: May 20, 2025

Language: Английский

Citations

0
Emerging role of m6A modification in fibrotic diseases and its potential therapeutic effect DOI

Wufei Ye,

Xiongwen Lv,

Songsen Gao

et al.

Biochemical Pharmacology, Journal Year: 2023, Volume and Issue: 218, P. 115873 - 115873

Published: Oct. 24, 2023

Language: Английский

Citations

8
Unravelling the impact of RNA methylation genetic and epigenetic machinery in the treatment of cardiomyopathy DOI Creative Commons
Li Liu,

Linxing Yu,

Y Wang

et al.

Pharmacological Research, Journal Year: 2024, Volume and Issue: 207, P. 107305 - 107305

Published: July 11, 2024

Cardiomyopathy (CM) represents a heterogeneous group of diseases primarily affecting cardiac structure and function, with genetic epigenetic dysregulation playing pivotal role in its pathogenesis. Emerging evidence from the burgeoning field epitranscriptomics has brought to light significant impact various RNA modifications, notably N6-methyladenosine (m6A), 5-methylcytosine (m5C), N7-methylguanosine (m7G), N1-methyladenosine (m1A), 2′-O-methylation (Nm), 6,2′-O-dimethyladenosine (m6Am), on cardiomyocyte function broader processes vascular remodelling. These modifications have been shown influence key pathological mechanisms including mitochondrial dysfunction, oxidative stress, apoptosis, inflammation, immune response, myocardial fibrosis. Importantly, aberrations methylation machinery observed human CM cases animal models, highlighting critical methylating enzymes their potential as therapeutic targets or biomarkers for CM. This review underscores necessity deeper understanding context CM, illuminate novel avenues diagnostic tools, thereby addressing gap current management strategies this complex disease.

Language: Английский

Citations

2