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 role and mechanism of m6A methylation in diabetic nephropathy DOI
Lin-Jing Yan, Liang Guo

Life Sciences, Journal Year: 2025, Volume and Issue: 363, P. 123355 - 123355

Published: Jan. 6, 2025

Language: Английский

Citations

1
Balancing inflammation: the specific roles of serum amyloid A proteins in sterile and infectious diseasese DOI Creative Commons
Tirthankar Mohanty, Katarina Miličević,

Henri Göthert

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: Feb. 10, 2025

Serum Amyloid A (SAA) proteins are acute-phase reactants with critical roles in sterile and bacterial inflammation. Through vitro vivo experiments, we demonstrate that SAA amplify cytokine chemokine responses during inflammation enhance clearance infectious conditions. Mechanistically, augment NF-κB signaling, driving pro anti-inflammatory mediator production. SAA-/- mice carrying a deletion of the Saa1, Saa2, Saa3, Saa4 serum amyloid genes have better survival rates sepsis but more prone to than their SAA+/+ counterparts, emphasizing dual functionality immune regulation. Overexpression macrophages enhances NF-κB-mediated pro-inflammatory production infection. Together, our results show key modulators inflammation, distinct mechanisms tailored contexts.

Language: Английский

Citations

1
Vaccarin ameliorates osteoarthritis by suppressing the c-Jun N-terminal kinase (JNK)-serum amyloid A2 (SAA2) pathway mediating chondrocyte senescence DOI Creative Commons
Xin Gan, Jianwen Li,

Yongqiao Jiang

et al.

Phytomedicine, Journal Year: 2025, Volume and Issue: unknown, P. 156697 - 156697

Published: March 1, 2025

Osteoarthritis is a chronic degenerative joint disease marked by chondrocyte senescence and extracellular matrix degradation. Vaccarin, flavonoid with anti-inflammatory antioxidant properties, has not been previously investigated for its therapeutic potential in osteoarthritis. To evaluate the of Vaccarin osteoarthritis elucidate underlying mechanisms. This study utilized vitro cultures RNA sequencing to identify relevant pathways, followed validation at genetic, protein, metabolic levels using multiple approaches. Additionally, effects were assessed vivo destabilization medial meniscus (DMM)-induced mouse model human cartilage samples from patients. effectively ameliorated both vitro. Transcriptomic indicated significant downregulation serum amyloid A2 (SAA2) expression following treatment. Multi-omics analysis, validated specimens, that SAA2 minimally secreted healthy articular but serves as crucial biomarker Asian populations. Mechanistically, inhibits c-Jun N-terminal kinase (JNK) phosphorylation, thereby reducing mitigating inflammation senescence. Notably, inflammatory conditions upregulate chondrocytes via JNK pathway. Elevated contribute mitochondrial dysfunction chondrocytes, leading increased reactive oxygen species (ROS) production exacerbating progression. identifies target suggests presents promising treatment avenue.

Language: Английский

Citations

0
Landscape analysis of m6A modification regulators reveals LRPPRC as a key modulator in tubule cells for DKD: a multi-omics study DOI Creative Commons
Li Jiang, Haijun Yu,

Jie Jian

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: April 4, 2025

Background Diabetic Kidney Disease (DKD) is a serious complication of diabetes, imposing substantial medical burden. The significance N6-methyladenosine (m6A) modification in the pathogenesis DKD has become increasingly prominent. Aim This study aimed to investigate specific expression patterns m6A geneset DKD. Method Bulk RNA, single-cell and spatial transcriptome were utilized clarify hub gene. 3 types machine learning algorithms applied. possible compounds screened based on DSigDB database. Result GSEA revealed potential m6a-associated pathways such as cGMP-PKG pathway. GSVA showed that two m6a regulation, namely m6a-readers m6a-writers, generally suppressed patients. output algorithm differential analysis determined LRPPRC was downregulated LOH, PODO, CT, CD-ICB cell populations, most which tubular cells. It exhibited decreasing trend over time, particularly pronounced LOH low activity mainly detected injured renal tubules. In clinical patients, levels mRNA tendency be correlations with Glomerular Filtration Rate (GFR) proteinuria according Nephroseq lobeline might an important compound involved regulation other genes. Its actual efficacy needs verified vivo or vitro .

Language: Английский

Citations

0
N6-methyladenine RNA methylation epigenetic modification and diabetic microvascular complications DOI Creative Commons
Yuanyuan Wang,

Jiayun Zou,

Hua Zhou

et al.

Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15

Published: Sept. 4, 2024

N6-methyladensine (m

Language: Английский

Citations

2
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

Citations

0