Epitranscriptomic regulations in the heart DOI Creative Commons

D Benak,

František Kolář, Markéta Hlaváčková

et al.

Physiological Research, Journal Year: 2024, Volume and Issue: unknown

Published: March 22, 2024

RNA modifications affect key stages of the life cycle, including splicing, export, decay, and translation. Epitranscriptomic regulations therefore significantly influence cellular physiology pathophysiology. Here, we selected some most abundant reviewed their roles in heart cardiovascular diseases: N6-methyladenosine (m6A), N6,2'-O-dimethyladenosine (m6Am), N1-methyladenosine (m1A), pseudouridine (?), 5 methylcytidine (m5C), inosine (I). Dysregulation epitranscriptomic machinery affecting these vastly changes cardiac phenotype is linked with many diseases such as myocardial infarction, cardiomyopathies, or failure. Thus, a deeper understanding regulatory mechanisms can enhance our knowledge molecular underpinnings prevalent diseases, potentially paving way for novel therapeutic strategies. Keywords: Epitranscriptomics, modifications, Epigenetics, m6A, RNA, Heart.

Language: Английский

N6-methyladenosine RNA methylation in diabetic kidney disease DOI Creative Commons

Jiaan Huang,

Fan Yang,

Yan Liu

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 171, P. 116185 - 116185

Published: Jan. 18, 2024

Diabetic kidney disease (DKD) is a major microvascular complication of diabetes, and hyperglycemic memory associated with diabetes carries the risk occurrence, even after termination blood glucose injury. The existence supports concept an epigenetic mechanism involving n6-methyladenosine (m6A) modification. Several studies have shown that m6A plays key role in pathogenesis DKD. This review addresses RNA modification progression DKD, including regulatory pathological processes, such as inflammation, oxidative stress, fibrosis, non-coding (nc) RNA. reveals importance occurrence development suggesting may play phenomenon. also discusses how some gray areas, modified multiple enzymes, interact to affect DKD provides countermeasures. In conclusion, this enhances our understanding from perspective modifications new targets for future therapeutic strategies. addition, insights discussed here support effects which far-reaching implications novel treatments. We hypothesize modification, factor regulating in-depth exploration option clinical management patients

Language: Английский

Citations

9

Molecular mechanisms of m6A modifications regulating tumor radioresistance DOI Creative Commons

Ruolin Shen,

Zhenyang Jiang,

Huanhuan Wang

et al.

Molecular Medicine, Journal Year: 2025, Volume and Issue: 31(1)

Published: Feb. 19, 2025

Abstract Radiotherapy is one of the most effective treatments for malignant tumors. Radioresistance a major factor that contributes to radiotherapy failure and poor prognosis. Recent studies have elucidated pivotal role aberrant N6-methyladenosine (m6A) modification, predominant internal mRNA modification in eukaryotic cells, influences cancer progression by disrupting gene expression other critical cellular processes. Furthermore, m6A methylation provides substrate tumor therapy; however, whether it regulates radioresistance remains unclear. Methylated transferase (writer), demethylated (eraser), methylated recognition protein (reader) are three essential proteins regulate via different mechanisms This review summarizes latest research advances aims provide novel perspectives on advancement regimens overcome invasion.

Language: Английский

Citations

1

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

Daniel Benák,

František Kolář, Lu Zhang

et al.

Epigenetics, Journal Year: 2023, Volume and Issue: 18(1)

Published: June 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.

Language: Английский

Citations

16

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

Min Zhang,

Jun Shi, Jun Zhou

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2023, Volume and Issue: 262, P. 115174 - 115174

Published: June 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.

Language: Английский

Citations

13

Epigenetic regulation of programmed cell death in hypoxia-induced pulmonary arterial hypertension DOI Creative Commons
Yuan Jiang,

Shasha Song,

Jingxin Liu

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Sept. 11, 2023

Pulmonary arterial hypertension (PAH) is a severe progressive disease that may cause early right ventricular failure and eventual cardiac failure. The pathogenesis of PAH involves endothelial dysfunction, aberrant proliferation pulmonary artery smooth muscle cells (PASMCs), vascular fibrosis. Hypoxia has been shown to induce elevated secretion growth factor (VEGF), leading the development hypoxic PAH. However, molecular mechanisms underlying remain incompletely understood. Programmed cell death (PCD) natural regulated by certain genes. Emerging evidence suggests apoptotic resistance contributes Moreover, several novel types PCD, such as autophagy, pyroptosis, ferroptosis, have reported be involved in Additionally, multiple diverse epigenetic including RNA methylation, DNA histone modification, non-coding molecule-mediated processes strongly linked These modifications affect expression genes, which produce important changes cellular biological processes, PCD. Consequently, better understanding PCD modification will provide novel, specific therapeutic strategies for diagnosis treatment. In this review, we aim discuss recent advances elucidate role regulating hypoxia-induced

Language: Английский

Citations

13

RNA m6A methylation and regulatory proteins in pulmonary arterial hypertension DOI
Zhe Wang, Yixuan Zhang,

Jun-Zhuo Shi

et al.

Hypertension Research, Journal Year: 2024, Volume and Issue: 47(5), P. 1273 - 1287

Published: March 4, 2024

Language: Английский

Citations

4

WTAP suppresses STAT3 via m6A methylation to regulate autophagy and inflammation in central nervous system injury DOI Creative Commons
Xiaoyong Zhao, Xiaoli Zhang, Liangzhi Wu

et al.

Neurobiology of Disease, Journal Year: 2025, Volume and Issue: unknown, P. 106811 - 106811

Published: Jan. 1, 2025

Language: Английский

Citations

0

M6a demethylase FTO regulates the oxidative stress, mitochondrial biogenesis of cardiomyocytes and PGC-1a stability in myocardial ischemia-reperfusion injury DOI Creative Commons
Qiong Jiang, Xuehai Chen,

Kezeng Gong

et al.

Redox Report, Journal Year: 2025, Volume and Issue: 30(1)

Published: Jan. 27, 2025

Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI discovering new targets are crucial for future treatment MIRI. We constructed rat model hypoxia/reoxygenation (H/R) cardiomyocytes model. RT-PCR Western blot were used to investigate expression fat mass obesity-associated (FTO) gene. Electrocardiogram, echocardiography, triphenyltetrazolium chloride (TTC) staining hematoxylin-eosin (HE) assess effect FTO overexpression. The generation reactive oxygen species (ROS) levels superoxide dismutase (SOD2), mitochondrial transcription factor (TFAM) cytochrome c oxidase I (COXI) detected oxidative stress biogenesis. RNA immunoprecipitation (RIP) pulldown assays identify interaction PGC-1a. m6A dot blot, methylated PCR (MeRIP-PCR) stability analysis analyze regulation methylation PGC-1a by FTO. was downregulated in rats H/R induced cardiomyocytes. Overexpression inhibited ROS level increased SOD2, TFAM COXI vitro vivo. In addition, identified as downstream target enhanced mRNA through removing modification. Our study revealed role regulates biogenesis via MIRI, which may provide approach mitigating

Language: Английский

Citations

0

METTL14-mediated m 6 A modification of DDIT4 promotes its mRNA stability in aging-related idiopathic pulmonary fibrosis DOI Creative Commons
Dan Li, Qian Li,

Yufeng Du

et al.

Epigenetics, Journal Year: 2025, Volume and Issue: 20(1)

Published: Feb. 7, 2025

Although N6-methyladenosine (m6A) may be related to the pathogenesis of fibrotic process, mechanism m6A modification in aging-related idiopathic pulmonary fibrosis (IPF) remains unclear. Three-milliliter venous blood was collected from IPF patients and healthy controls. MeRIP-seq RNA-seq were utilized investigate differential modification. The expressions identified regulator target gene validated using MeRIP-qPCR real-time PCR. Moreover, we established an animal model a senescent A549 cells explore associated molecular mechanism. Our study provided panorama methylation IPF. Increased peaks (3756) decreased (4712) observed group. association analysis showed that 749 DEGs affected by Among regulators, expression METTL14 level our interested DDIT4 significantly, but mRNA higher This further verified bleomycin-induced fibrosis. At cellular level, it confirmed might participate senescence alveolar epithelial cells. downregulation inhibit decay reducing mRNA, leading high protein. alterations discovered as potential intervention for epigenetic These results pave way future investigations regarding modifications

Language: Английский

Citations

0

[Research progress on N6-methyladenosine and ferroptosis in childhood combined allergic rhinitis and asthma syndrome]. DOI
Jing Li, Yujian Li,

Sheng-Lin Lai

et al.

PubMed, Journal Year: 2025, Volume and Issue: 27(2), P. 242 - 247

Published: Feb. 15, 2025

Combined allergic rhinitis and asthma syndrome (CARAS) is one of the common chronic airway inflammatory diseases in children. With development epigenetics, research on CARAS has gradually extended from protein levels to molecular levels, such as transcription post-transcriptional regulation. N6-methyladenosine (m6A) methylation ferroptosis have emerged promising hotspots recent years, playing crucial roles tumors, growth development, diseases. This paper aims summarize characteristics m6A ferroptosis, along with their onset progression children, thereby providing new insights strategies for diagnosis treatment childhood CARAS.

Language: Английский

Citations

0