Non-coding RNA Research最新文献

{"title":"Long non-coding RNAs in humans: Classification, genomic organization and function","authors":"Barbara Chodurska ,&nbsp;Tanja Kunej","doi":"10.1016/j.ncrna.2025.01.004","DOIUrl":"10.1016/j.ncrna.2025.01.004","url":null,"abstract":"<div><div>Long non-coding RNAs (lncRNAs) regulate numerous biological functions in animals. Despite recent advances in lncRNA research, their structural and functional annotation and classification remain an ongoing challenge. This review provides a comprehensive overview of human lncRNAs, highlighting their genomic organization, mode of action and role in physiological and pathological processes. Subgroups of lncRNA genes are discussed using representative examples and visualizations of genomic organization. The HUGO Gene Nomenclature Committee (HGNC) categorizes lncRNAs into nine subgroups: (1) microRNA non-coding host genes, (2) small nucleolar RNA non-coding host genes, (3) long intergenic non-protein coding RNAs (LINC), (4) antisense RNAs, (5) overlapping transcripts, (6) intronic transcripts, (7) divergent transcripts, (8) long non-coding RNAs with non-systematic symbols and (9) long non-coding RNAs with FAM root systems. Circular RNAs (circRNAs) are a separate class that shares some characteristics with lncRNAs and are divided into exonic, intronic and intronic-exonic types. LncRNAs act as molecular signals, decoys, scaffolds and sponges for microRNAs and often function as competing endogenous RNAs (ceRNAs). LncRNAs are involved in various physiological and pathological processes, such as cell differentiation, p53-mediated DNA damage response, glucose metabolism, inflammation and immune functions. They are associated with several diseases, including various types of neoplasms, Alzheimer's disease and autoimmune diseases. A clear classification system for lncRNA is essential for understanding their biological role and for facilitating practical applications in biomedical research. Future studies should focus on drug development and biomarker discovery. As important regulators of various biological processes, lncRNAs represent promising targets for innovative therapies.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 313-327"},"PeriodicalIF":5.9,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143129811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA-mRNA regulatory network reveals key lncRNAs tightly associated with preterm labor and premature rupture of membranes","authors":"Guangqiong Yang,&nbsp;Wenjin Qi","doi":"10.1016/j.ncrna.2025.01.002","DOIUrl":"10.1016/j.ncrna.2025.01.002","url":null,"abstract":"<div><div>Premature rupture of membranes (PROM) and preterm birth (PTB) are significant pregnancy complications, accounting for approximately one-third of PTB, often preceded by preterm PROM (PPROM). The underlying causes of PROM and PTB are multifaceted and not fully understood. Long non-coding RNAs (lncRNAs) have emerged as pivotal elements in the molecular landscape of PPROM. In our study, we analyzed fetal membrane samples from Term labor (TL), PROM, PTB, and PPROM groups using transcriptome sequencing to identify differentially expressed genes, including both lncRNAs and mRNAs. Our findings highlighted a subset of lncRNAs, BBOX1-AS1, VIM-AS1, XLOC-031812 and AC106706.1 as potentially influential in the pathophysiology of PROM and PTB. Co-expression analyses further revealed that the target genes regulated by these lncRNAs were significantly implicated in pregnancy progression and embryonic placental development. These insights underscored the importance of the lncRNA-mRNA axis in the onset and progression of PROM and PTB, offering new avenues for understanding the molecular mechanisms underlying these conditions. Our research not only contributes to the elucidation of lncRNA mediated regulatory mechanisms in PROM and PTB, but also holds promise for improving preventative and therapeutic strategies, ultimately safeguarding maternal and infant well-being.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 273-280"},"PeriodicalIF":5.9,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143129197","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibition of MALAT1 facilitates ROS accumulation via the Keap1/HO-1 pathway to enhance photodynamic therapy in secondary hyperparathyroidism","authors":"Ying Wen ,&nbsp;Yitong Li ,&nbsp;Danhua Zhang ,&nbsp;Ziru Liu ,&nbsp;Hong Liu ,&nbsp;Xiejia Li ,&nbsp;Wei Wu ,&nbsp;Liyun Zeng ,&nbsp;Qiongyan Zou ,&nbsp;Wenjun Yi","doi":"10.1016/j.ncrna.2024.12.001","DOIUrl":"10.1016/j.ncrna.2024.12.001","url":null,"abstract":"<div><div>The prevalence of secondary hyperparathyroidism (SHPT) in advanced chronic kidney disease (CKD) exceeds 80 %. Our previous study indicated that photodynamic therapy (PDT) has potential for treating SHPT. Long noncoding RNA (lncRNA) is involved in various oxidative stress and apoptotic processes, but the molecular mechanism remains unreported. In this study, we found that PDT induced apoptosis in SHPT through reactive oxygen species (ROS) accumulation. The expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and heme oxygenase 1 (HO-1) within SHPT was upregulated after PDT. Inhibition of MALAT1 increased PDT-induced ROS, which promoted the apoptosis. Pearson correlation analysis confirmed that there was a positive correlation between MALAT1 and HO-1, and MALAT1 inhibition down-regulated HO-1, whereas concomitant overexpression of HO-1 was able to eliminate the PDT-induced ROS and inhibit apoptosis. The direct binding of MALAT1 to Kelch-like ECH-associated protein 1 (Keap1) protein was confirmed by high-throughput sequencing, RNA pulldown, silver staining and western blotting assays. Si-Keap1 was able to rescue the down-regulation of HO-1 caused by MALAT1 inhibition, restoring the elimination of ROS by HO-1 and attenuating the effect of PDT. In addition, PDT effectively reduced parathyroid hormone (PTH) secretion in SHPT rats, and this effect was further enhanced in combination with MALAT1 inhibitors. Overall, MALAT1 activates downstream HO-1 expression by binding to Keap1, thereby reducing ROS and inhibiting apoptosis, which in turn mediates PDT resistance in SHPT. Inhibition of MALAT1 significantly enhanced the efficacy of PDT, suggesting a potential therapeutic target for improving PDT for SHPT outcomes.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 249-261"},"PeriodicalIF":5.9,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum/glucose starvation enhances binding of miR-4745-5p and miR-6798-5p to HNRNPA1 mRNA 3ʹUTR: A novel method to identify miRNAs binding to mRNA 3ʹUTR using λN peptide-boxB sequence","authors":"Tetsuyuki Takahashi,&nbsp;Mai Funamura,&nbsp;Shun Wakai,&nbsp;Takao Hijikata","doi":"10.1016/j.ncrna.2025.01.001","DOIUrl":"10.1016/j.ncrna.2025.01.001","url":null,"abstract":"<div><div>Serum/glucose starvation causes complete loss of heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) without altering mRNA levels. However, the mechanisms driving hnRNP A1 downregulation during serum/glucose starvation are not yet well understood. Using the novel interaction between the λN peptide and boxB sequence (λN/boxB system) and miRNA microarray analysis, we aimed to identify specific-binding microRNAs (miRs or miRNAs) targeting <em>HNRNPA1</em> mRNA 3ʹUTR under serum/glucose-starved conditions. Four miRNAs were identified as serum/glucose starvation-driven miRNAs for <em>HNRNPA1</em> mRNA 3ʹUTR. Reporter assays, anti-miRNA and mutated miRNA-based assays, photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation/reverse transcribed-quantitative polymerase chain reaction, and transient overexpression of miRNAs showed that miR-4745-5p and miR-6798-5p suppress hnRNP A1 protein levels via enhancement of binding to <em>HNRNPA1</em> mRNA 3ʹUTR under serum/glucose-starved condition. miR-4745-5p and miR-6798-5p overexpression significantly decreased growth rates, which was rescued by co-transfection with anti-miRNA for miR-4745-5p and miR-6798-5p. Anti-miRNA transfection for miR-4745-5p and miR-6798-5p significantly increased growth rates under serum/glucose-starved conditions. Furthermore, hnRNP A1 overexpression recovered miR-4745-5p- and miR-6798-5p-induced growth suppression. These findings indicated that miR-4745-5p and miR-6798-5p are serum/glucose starvation-driven miRNAs for hnRNP A1 and validated the λN/boxB system as a simple and useful method for detecting mRNA 3ʹUTR-bound miRNA.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 188-199"},"PeriodicalIF":5.9,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786793/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081591","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNA NEAT1-206 regulates autophagy of human umbilical cord mesenchymal stem cells through the WNT5A/Ca2+ signaling pathway under senescence stress","authors":"Weili Wang ,&nbsp;Yongyu Wang ,&nbsp;Chunchun Duan ,&nbsp;Wenjing Tian ,&nbsp;Liyang Gao","doi":"10.1016/j.ncrna.2024.12.013","DOIUrl":"10.1016/j.ncrna.2024.12.013","url":null,"abstract":"<div><div>Stem cells are crucial for maintaining bodily stability, but their regenerative abilities decline with age. This decline is marked by reduced proliferation and differentiation capacities of stem cells, as well as exhaustion of the stem cell pool. The accumulation of aged mesenchymal stem cells (MSCs) can reduce the tissue regeneration, but the molecular mechanisms influencing MSCs aging remain unclear. Moreover, collecting MSCs from elderly individuals is not suitable for observing the early response of MSCs to senescence stress, and the factors involved in early senescence remain unclear. In our previous study, we established a fast MSC aging model using D-galactose. We discovered that, while not affecting the \"stemness\" markers of mesenchymal stem cells, the expression of LncRNA NEAT1-206 was notably increased during the early stages of aging induction (within 4 days). And LncRNA NEAT1-206 was observed to be localized in the cytoplasmic matrix due to enhanced nuclear export. We found that the LncRNA NEAT1-206 could trigger autophagy through the WNT5A/Ca²⁺ signaling pathway, thereby decreasing senescence markers and enhancing the osteogenic differentiation of MSCs. This study elucidated the role that LncRNA NEAT1-206 as a potential key factor in conferring resistance to D-galactose-induced cell senescence at the early stage and promoting the osteogenic differentiation of MSCs. This study may provide a foundational understanding for delaying the MSCs aging process.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 234-248"},"PeriodicalIF":5.9,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786084/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and validation of lncRNA mutation hotspot SNPs associated with myasthenia gravis susceptibility","authors":"Ni He ,&nbsp;Liting Tian ,&nbsp;Jingnan Jin ,&nbsp;Yue Liu ,&nbsp;Lifang Li ,&nbsp;Xiaokun Wang ,&nbsp;Danyang Li ,&nbsp;Xia Wang ,&nbsp;Xiaoju Li ,&nbsp;Zihong Chen ,&nbsp;Lanxin Zhang ,&nbsp;Lukuan Qiao ,&nbsp;Shangwei Ning ,&nbsp;Lihua Wang ,&nbsp;Jianjian Wang","doi":"10.1016/j.ncrna.2024.12.012","DOIUrl":"10.1016/j.ncrna.2024.12.012","url":null,"abstract":"<div><h3>Background</h3><div>Myasthenia gravis (MG) is an autoimmune disorder caused by antibodies that target the postsynaptic muscle membrane. Recent evidence suggests that genetic variants and long noncoding RNAs (lncRNAs) play crucial roles in the pathogenesis of MG. The purpose of this study was to investigate the associations between lncRNA-related single-nucleotide polymorphisms (SNPs) and MG susceptibility in Chinese populations.</div></div><div><h3>Methods</h3><div>First, we identified lncRNA mutation hotspot regions based on the improved Kolmogorov‒Smirnov test and the cumulative hypergeometric distribution principle. Next, we further identified lncRNA mutation hotspot SNPs by calculating conservative scores. Finally, experiments were conducted to verify the associations between lncRNA mutation hotspot SNPs and MG susceptibility. A total of 82 patients with MG and 82 healthy controls were recruited for genotyping of lncRNA mutation hotspot SNPs using the SNaPshot technique. Quantitative real-time PCR was used to investigate lncRNA expression in 34 patients with MG and 37 healthy controls.</div></div><div><h3>Results</h3><div>In the multistep calculation, 14 candidate SNPs of 3 lncRNAs (AL031686.1, NONHSAT028539.2 and AC245014.3) in MG were identified as mutation hotspot SNPs. The genotyping results of the 14 SNPs in our study revealed no statistically significant differences in the frequencies of genotypes and alleles between patients with MG and controls. However, in the lncRNA AL031686.1, rs1000383 and rs6094353 were in perfect linkage disequilibrium (LD) and were associated with an increased risk of ocular MG. Additionally, rs6094347 was associated with an increased risk of ocular MG. Nevertheless, no SNP was found to be associated with factors such as sex, age, the presence or absence of thymoma, or the genetic model of MG. Further experiments revealed that NONHSAT028539.2 expression was upregulated in peripheral blood mononuclear cells (PBMCs) from patients with MG compared with those from healthy controls.</div></div><div><h3>Conclusion</h3><div>In our study, we did not find an association between the 14 mutation hotspot SNPs of lncRNAs and susceptibility to MG. However, we observed that the rs6094347 and rs1000383/rs6094353 polymorphisms in the lncRNA AL031686.1 were associated with the risk of ocular MG.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 209-219"},"PeriodicalIF":5.9,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances of miR-23 in human diseases and growth development","authors":"Xu Qian ,&nbsp;Yongwei Jiang ,&nbsp;Yadi Yang ,&nbsp;Yukun Zhang ,&nbsp;Na Xu ,&nbsp;Bin Xu ,&nbsp;Ke Pei ,&nbsp;Zhi Yu ,&nbsp;Wei Wu","doi":"10.1016/j.ncrna.2024.12.010","DOIUrl":"10.1016/j.ncrna.2024.12.010","url":null,"abstract":"<div><div>MicroRNA (miRNA) is broadly manifested in eukaryotes and serves as a critical function in biological development and disease occurrence. With the rapid advancement of experimental research tools, researchers have discovered functional correlations among different miRNA isoforms and clusters within the same miRNA family. As a highly conserved member in the miR-23-27-24 cluster, miR-23 exhibits different isoforms and participates in various essential development. Although the miR-23-27-24 cluster has overlapping target sites, their differential expression can demonstrate independent biological functions. Furthermore, the untapped effects of miR-23 on organisms, whether as a functional cluster or a single regulator, has not been systematically elucidated yet. In this review article, we analyze the genomic location of miR-23 and its sequence variances among its isoforms or family members while summarizing its regulatory functions in metabolic diseases, immune responses, cardiovascular diseases, cancer, organ development as well as nervous system function. This review highlights the significant role of miR-23 as a biomarker for disease diagnosis and a key regulatory factor in pathogenesis, which can help us comprehend the diverse functions of miRNAs and provide a theoretical reference for the functional differences among miRNA isoforms.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 220-233"},"PeriodicalIF":5.9,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11787465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of tRNA-Derived small RNAs (tsRNAs) in pancreatic cancer and acute pancreatitis","authors":"Yan Pan ,&nbsp;Xiaowei Ying ,&nbsp;Xueting Zhang ,&nbsp;Hongting Jiang ,&nbsp;Junjie Yan ,&nbsp;Shiwei Duan","doi":"10.1016/j.ncrna.2024.12.011","DOIUrl":"10.1016/j.ncrna.2024.12.011","url":null,"abstract":"<div><div>tRNA-derived small RNAs (tsRNAs), encompassing tRNA fragments (tRFs) and tRNA-derived stress-induced RNAs (tiRNAs), represent a category of non-coding small RNAs (sncRNAs) that are increasingly recognized for their diverse biological functions. These functions include gene silencing, ribosome biogenesis, retrotransposition, and epigenetics. tsRNAs have been identified as key players in the progression of various tumors, yet their specific roles in pancreatic cancer (PC) and acute pancreatitis (AP) remain largely unexplored. Pancreatic cancer, particularly pancreatic ductal adenocarcinoma, is notorious for its high mortality rate and extremely low patient survival rate, primarily due to challenges in early diagnosis. Similarly, acute pancreatitis is a complex and significant disease. This article reviews the roles of 18 tsRNAs in PC and AP, focusing on their mechanisms of action and potential clinical applications in these two diseases. These tsRNAs influence the progression of pancreatic cancer and acute pancreatitis by modulating various pathways, including ZBP1/NLRP3, Hippo, PI3K/AKT, glycolysis/gluconeogenesis, and Wnt signaling. Notably, the dysregulation of tsRNAs is closely linked to critical clinical factors in pancreatic cancer and acute pancreatitis, such as lymph node metastasis, tumor-node-metastasis (TNM) stage, overall survival (OS), and disease-free survival (DFS). This article not only elucidates the mechanisms by which tsRNAs affect pancreatic cancer and acute pancreatitis but also explores their potential as biomarkers and therapeutic targets for pancreatic cancer. The insights provided here offer valuable references for future research, highlighting the importance of tsRNAs in the diagnosis and treatment of these challenging diseases.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 200-208"},"PeriodicalIF":5.9,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11786804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081611","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of long non-coding RNAs in cardiovascular diseases: A comprehensive review","authors":"Xuena Xie ,&nbsp;Meiwen Huang ,&nbsp;Shudong Ma ,&nbsp;Qiqi Xin ,&nbsp;Yuying Wang ,&nbsp;Lantian Hu ,&nbsp;Han Zhao ,&nbsp;Pengqi Li ,&nbsp;Mei Liu ,&nbsp;Rong Yuan ,&nbsp;Yu Miao ,&nbsp;Yizhun Zhu ,&nbsp;Weihong Cong","doi":"10.1016/j.ncrna.2024.12.009","DOIUrl":"10.1016/j.ncrna.2024.12.009","url":null,"abstract":"<div><div>Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide, posing significant challenges to healthcare systems. Despite advances in medical interventions, the molecular mechanisms underlying CVDs are not yet fully understood. For decades, protein-coding genes have been the focus of CVD research. However, recent advances in genomics have highlighted the importance of long non-coding RNAs (lncRNAs) in cardiovascular health and disease. Changes in lncRNA expression specific to tissues may result from various internal or external factors, leading to tissue damage, organ dysfunction, and disease. In this review, we provide a comprehensive discussion of the regulatory mechanisms underlying lncRNAs and their roles in the pathogenesis and progression of CVDs, such as coronary heart disease, atherosclerosis, heart failure, arrhythmias, cardiomyopathies, and diabetic cardiomyopathy, to explore their potential as therapeutic targets and diagnostic biomarkers.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 158-187"},"PeriodicalIF":5.9,"publicationDate":"2024-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11783329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143081608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long non-coding RNA AK023617 orchestrates atherosclerosis by regulating the circadian rhythm of immunity-related GTPase family M protein in macrophages","authors":"Rongzhe Lu ,&nbsp;Hengxuan Cai ,&nbsp;Yige Liu ,&nbsp;Guanpeng Ma ,&nbsp;Jiaxin Wang ,&nbsp;Miao Yan ,&nbsp;Zhenming Zhang ,&nbsp;Bo Yu ,&nbsp;Zhaoying Li ,&nbsp;Shaohong Fang","doi":"10.1016/j.ncrna.2024.12.008","DOIUrl":"10.1016/j.ncrna.2024.12.008","url":null,"abstract":"<div><div>Acute coronary events show a diurnal rhythm, and atherosclerotic plaque vulnerability, as a histomorphological characteristic of major adverse cardiovascular events, is a key target for intervention. Although oscillating microRNAs reduce plaque stability by facilitating macrophage apoptosis in lesions, whether rhythmic long non-coding RNA (lncRNA) can regulate diurnal oscillations in plaque stability and the potential underlying mechanism remain unclear. In this study, we examined whether rhythmic lncRNAs are involved in the pathogenesis and progression of atherosclerosis and detected a novel circadian lncRNA-AK023617, which is positively correlated with the peak occurrence of major adverse cardiovascular events. Transfection of short interfering RNA specific to lnc-AK023617 into THP-1 cells dampened the oscillation of immunity-related GTPase family M protein 1 (Irgm1), which is negatively related to plaque stability. In ApoE^−/− mice fed a high-fat diet for 12 weeks, diurnal variations in lncAK023617 were consistent with the proportions of necroptotic cells in atherosclerotic plaques. In addition, reduced expression of lncAK023617 inhibited P-RIP3 and P-MLKL in THP-1 cells. Mechanistically, lncAK023617 interacted with the core molecular clock Bmal1 and promoted nuclear translocation of Bmal1, which could directly bind to the E-BOX elements in the <em>Irgm1</em> promoter. Thus, oscillating lncAK023617 in macrophages can affect plaque stability by regulating necroptosis, which regulates circadian expression of the target gene <em>Irgm1</em> by increasing the transcriptional activity of Bmal1, ultimately determining the diurnal oscillations in plaque stability. Therefore, lncAK023617 may serve as a specific target to ameliorate atherosclerotic plaque vulnerability.</div></div>","PeriodicalId":37653,"journal":{"name":"Non-coding RNA Research","volume":"11 ","pages":"Pages 262-272"},"PeriodicalIF":5.9,"publicationDate":"2024-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11788686/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143123785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}