Frontiers in bioscience (Landmark edition)最新文献_第7页

Artificial Intelligence-Driven Precision Medicine: Multi-Omics and Spatial Multi-Omics Approaches in Diffuse Large B-Cell Lymphoma (DLBCL). 人工智能驱动的精准医学：弥漫性大b细胞淋巴瘤（DLBCL）的多组学和空间多组学方法。

IF 3.3

Frontiers in bioscience (Landmark edition) Pub Date : 2024-11-28 DOI: 10.31083/j.fbl2912404

Yanping Shao, Xiuyan Lv, Shuangwei Ying, Qunyi Guo

{"title":"Artificial Intelligence-Driven Precision Medicine: Multi-Omics and Spatial Multi-Omics Approaches in Diffuse Large B-Cell Lymphoma (DLBCL).","authors":"Yanping Shao, Xiuyan Lv, Shuangwei Ying, Qunyi Guo","doi":"10.31083/j.fbl2912404","DOIUrl":"https://doi.org/10.31083/j.fbl2912404","url":null,"abstract":"In this comprehensive review, we delve into the transformative role of artificial intelligence (AI) in refining the application of multi-omics and spatial multi-omics within the realm of diffuse large B-cell lymphoma (DLBCL) research. We scrutinized the current landscape of multi-omics and spatial multi-omics technologies, accentuating their combined potential with AI to provide unparalleled insights into the molecular intricacies and spatial heterogeneity inherent to DLBCL. Despite current progress, we acknowledge the hurdles that impede the full utilization of these technologies, such as the integration and sophisticated analysis of complex datasets, the necessity for standardized protocols, the reproducibility of findings, and the interpretation of their biological significance. We proceeded to pinpoint crucial research voids and advocated for a trajectory that incorporates the development of advanced AI-driven data integration and analytical frameworks. The evolution of these technologies is crucial for enhancing resolution and depth in multi-omics studies. We also emphasized the importance of amassing extensive, meticulously annotated multi-omics datasets and fostering translational research efforts to connect laboratory discoveries with clinical applications seamlessly. Our review concluded that the synergistic integration of multi-omics, spatial multi-omics, and AI holds immense promise for propelling precision medicine forward in DLBCL. By surmounting the present challenges and steering towards the outlined futuristic pathways, we can harness these potent investigative tools to decipher the molecular and spatial conundrums of DLBCL. This will pave the way for refined diagnostic precision, nuanced risk stratification, and individualized therapeutic regimens, ushering in a new era of patient-centric oncology care.","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"404"},"PeriodicalIF":3.3,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Identification and Characterisation of Potential Targets for N6-methyladenosine (m6A) Modification during Intervertebral Disc Degeneration. 椎间盘退变过程中n6 -甲基腺苷（m6A）修饰的潜在靶点的鉴定和表征。

IF 3.3

Frontiers in bioscience (Landmark edition) Pub Date : 2024-11-28 DOI: 10.31083/j.fbl2912405

Jianlin Shen, Qiang Zhang, Yujian Lan, Qingping Peng, Ziyu Ji, Yanjiao Wu, Huan Liu

{"title":"Identification and Characterisation of Potential Targets for N6-methyladenosine (m6A) Modification during Intervertebral Disc Degeneration.","authors":"Jianlin Shen, Qiang Zhang, Yujian Lan, Qingping Peng, Ziyu Ji, Yanjiao Wu, Huan Liu","doi":"10.31083/j.fbl2912405","DOIUrl":"https://doi.org/10.31083/j.fbl2912405","url":null,"abstract":"Background: The mechanism for RNA methylation during disc degeneration is unclear. The aim of this study was to identify N6-methyladenosine (m6A) markers and therapeutic targets for the prevention and treatment of intervertebral disc degeneration (IDD).Methods: Methylated RNA immunoprecipitation sequencing (MeRIP-seq) and quantitative reverse transcription PCR (RT-qPCR) were employed to analyze m6A modifications of IDD-related gene expression. Bioinformatics was used to identify enriched gene pathways in IDD. m6A-RIP-qPCR was used to validate potential targets and markers.Results and conclusion: Human IDD samples exhibited a distinct m6A modification pattern that allowed associated genes and pathways to be identified. These genes had functions such as \"nuclear factor kappa-B (NF-κB) binding\" and \"extracellular matrix components\", which are crucial for IDD pathogenesis. ANXA2 showed increased m6A modification in IDD, while SLC3A2 and PBX3 showed decreased m6A methylation. The results of this study offer novel insights for the prevention and treatment of IDD.","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"405"},"PeriodicalIF":3.3,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epigenetic Modulations of Non-Coding RNAs: A Novel Therapeutic Perspective in Sjӧgren's Syndrome. 非编码rna的表观遗传调控：Sjӧgren综合征的新治疗视角。

IF 3.3

Frontiers in bioscience (Landmark edition) Pub Date : 2024-11-27 DOI: 10.31083/j.fbl2912403

Margherita Sisto, Sabrina Lisi

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Effects of Extracellular Matrix Changes Induced by a High-Fat Diet on Gallbladder Smooth Muscle Dysfunction. 高脂肪饮食诱导的细胞外基质改变对胆囊平滑肌功能障碍的影响。

IF 3.3

Frontiers in bioscience (Landmark edition) Pub Date : 2024-11-27 DOI: 10.31083/j.fbl2912401

Xingguo Zhong, Feiyang Wu, Weicheng Gao, Jinlong Hu, Bing Shen, Kaiyuan Zhong, Junbin Peng, Chong Zhang, Chao Zhang

{"title":"Effects of Extracellular Matrix Changes Induced by a High-Fat Diet on Gallbladder Smooth Muscle Dysfunction.","authors":"Xingguo Zhong, Feiyang Wu, Weicheng Gao, Jinlong Hu, Bing Shen, Kaiyuan Zhong, Junbin Peng, Chong Zhang, Chao Zhang","doi":"10.31083/j.fbl2912401","DOIUrl":"https://doi.org/10.31083/j.fbl2912401","url":null,"abstract":"Background: Gallstone formation is a common digestive ailment, with unclear mechanisms underlying its development. Dysfunction of the gallbladder smooth muscle (GSM) may play a crucial role, particularly with a high-fat diet (HFD). This study aimed to investigate the effects of an HFD on GSM and assess how it alters contractility through changes in the extracellular matrix (ECM).Methods: Guinea pigs and C57BL/6 mice were fed either an HFD or normal diet (ND). Primary cultures of their (guinea pigs) gallbladder smooth muscle cells (GSMCs) were used for in vitro experiments. Histological stains, RNA-sequencing, bioinformatics analysis, three-dimensional tissue culture, real-time polymerase chain reaction (PCR), Western blot, atomic force microscopy, and muscle tension measurements were performed.Results: Histological evidence indicated structural changes in the gallbladder muscle layer and ECM collagen deposition in the HFD group. The HFD group also showed increased expression of collagen, integrin family, and matrix metalloproteinase (MMP) and the phosphoinositide 3-kinase (PI3K)-protein kinase B (PKB/Akt) signaling pathway. Compared with GSMCs cultured on Matrigel containing 1 mg/mL of collagen I, those cultured with 2 mg/mL showed a phenotype change from contractile to synthetic cells. Consistent with these findings, the HFD group also demonstrated increased ECM stiffness and decreased smooth muscle contractility.Conclusions: Our findings reveal a mechanism by which an HFD alters the ECM composition of the gallbladder muscle, activating the integrin/PI3K-Akt/MMP signaling pathway, thereby impacting GSMC phenotype and contractility. These insights enhance the understanding of gallstone formation mechanism and provide potential therapeutic targets to treat gallbladder dysfunction.","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"401"},"PeriodicalIF":3.3,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142903955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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The Warburg Effect: Is it Always an Enemy? 华宝效应：永远都是敌人吗？

IF 3.3

Frontiers in bioscience (Landmark edition) Pub Date : 2024-11-27 DOI: 10.31083/j.fbl2912402

Christos Papaneophytou

{"title":"The Warburg Effect: Is it Always an Enemy?","authors":"Christos Papaneophytou","doi":"10.31083/j.fbl2912402","DOIUrl":"10.31083/j.fbl2912402","url":null,"abstract":"The Warburg effect, also known as 'aerobic' glycolysis, describes the preference of cancer cells to favor glycolysis over oxidative phosphorylation for energy (adenosine triphosphate-ATP) production, despite having high amounts of oxygen and fully active mitochondria, a phenomenon first identified by Otto Warburg. This metabolic pathway is traditionally viewed as a hallmark of cancer, supporting rapid growth and proliferation by supplying energy and biosynthetic precursors. However, emerging research indicates that the Warburg effect is not just a strategy for cancer cells to proliferate at higher rates compared to normal cells; thus, it should not be considered an 'enemy' since it also plays complex roles in normal cellular functions and/or under stress conditions, prompting a reconsideration of its purely detrimental characterization. Moreover, this review highlights that distinguishing glycolysis as 'aerobic' and 'anaerobic' should not exist, as lactate is likely the final product of glycolysis, regardless of the presence of oxygen. Finally, this review explores the nuanced contributions of the Warburg effect beyond oncology, including its regulatory roles in various cellular environments and the potential effects on systemic physiological processes. By expanding our understanding of these mechanisms, we can uncover novel therapeutic strategies that target metabolic reprogramming, offering new avenues for treating cancer and other diseases characterized by metabolic dysregulation. This comprehensive reevaluation not only challenges traditional views but also enhances our understanding of cellular metabolism's adaptability and its implications in health and disease.","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 12","pages":"402"},"PeriodicalIF":3.3,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142904138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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DLX5 Promotes Radioresistance in Renal Cell Carcinoma by Upregulating c-Myc Expression. DLX5通过上调c-Myc表达促进肾细胞癌放射耐药。

IF 3.3

Frontiers in bioscience (Landmark edition) Pub Date : 2024-11-26 DOI: 10.31083/j.fbl2911400

Danfei Hu, Mingyao Li, Xiaodong Chen

{"title":"DLX5 Promotes Radioresistance in Renal Cell Carcinoma by Upregulating c-Myc Expression.","authors":"Danfei Hu, Mingyao Li, Xiaodong Chen","doi":"10.31083/j.fbl2911400","DOIUrl":"https://doi.org/10.31083/j.fbl2911400","url":null,"abstract":"Background: Renal cell carcinoma (RCC) is a prevalent and aggressive kidney cancer with notable metastatic potential. While radiotherapy is effective for treating metastatic RCC, the emergence of radioresistance presents a major challenge. This study explores the role of DLX5, previously identified as an oncogene in various cancers, in the development of radioresistance in RCC.Methods: Distal-less homeobox 5 (DLX5) expression was measured using western blot analysis. To study the effects of DLX5, its expression was knocked down in 786-O and Caki-1 RCC cell lines through si-DLX5 transfection, and the impact of DLX5 on RCC cell proliferation and radioresistance was assessed using cell counting kit-8 (CCK-8), 5-Ethynyl-2'-deoxyuridine (EdU) incorporation assay, flow cytometry, colony formation, immunofluorescence, and western blot assays. The underlying mechanisms were explored through western blot, colony formation, and CCK-8 assays. In vivo effects were examined using a xenograft mouse model.Results: In silico results showed increased DLX5 levels in RCC tissues. Similarly, DLX5 expression was elevated in RCC cell lines. Silencing DLX5 reduced RCC cell proliferation and induced apoptosis in vitro. Additionally, DLX5 knockdown decreased radioresistance and increased DNA damage in RCC cells. Mechanistic studies revealed that DLX5 promotes radioresistance through the upregulation of c-Myc. In vivo, DLX5 silencing impeded tumor growth and reduced radioresistance.Conclusion: DLX5 contributes to RCC cell growth and radioresistance by upregulating c-Myc expression, highlighting its potential as a target for overcoming radioresistance in RCC.","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"400"},"PeriodicalIF":3.3,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Retraction: Huang Y, et al. Sophocarpine inhibits the growth of gastric cancer cells via autophagy and apoptosis. Frontiers in Bioscience-Landmark. 2019; 24: 616-627. 撤稿：黄颖，等。槐果碱通过自噬和凋亡抑制胃癌细胞的生长。生物科学前沿-里程碑。2019年;24: 616 - 627。

IF 3.3

Frontiers in bioscience (Landmark edition) Pub Date : 2024-11-22 DOI: 10.31083/j.fbl2911399

Frontiers In Bioscience-Landmark Editorial Office

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Effects of Arginine Vasopressin on Hippocampal Myelination in an Autism Rat Model: A RNA-seq and Mendelian Randomization Analysis. 精氨酸加压素对自闭症大鼠海马髓鞘形成的影响：RNA-seq和孟德尔随机化分析。

IF 3.3

Frontiers in bioscience (Landmark edition) Pub Date : 2024-11-21 DOI: 10.31083/j.fbl2911394

Xingxing Bao, Bo Zhou, Min Wen

{"title":"Effects of Arginine Vasopressin on Hippocampal Myelination in an Autism Rat Model: A RNA-seq and Mendelian Randomization Analysis.","authors":"Xingxing Bao, Bo Zhou, Min Wen","doi":"10.31083/j.fbl2911394","DOIUrl":"https://doi.org/10.31083/j.fbl2911394","url":null,"abstract":"Background: To explore the therapeutic role of arginine vasopressin (AVP) and its possible mechanisms in autism.Methods: Mid-trimester pregnant rats treated with valproate on embryonic day 12.5 and their offspring were selected as autism model. The autism rats were randomly assigned to autism group and AVP treatment group that given AVP by inhalation per day from postnatal days 21 to 42. The changes in social behavior and the hippocampus transcriptome were compared, and the hub genes were confirmed by quantitative real-time polymerase chain reaction (qPCR) and Mendelian randomization (MR).Results: 403 genes were found to be differentially expressed in the autism model, with the majority of these genes being involved in oligodendrocyte development and myelination. Only 11 genes associated with myelination exhibited statistically significant alterations following AVP treatment when compared to the autism group. Gene set enrichment, expression patterns, and weighted gene co-expression network analysis (WGCNA) analysis consistently indicated that the biological processes of oligodendrocyte development and myelination were markedly enriched in the autism group and exhibited improvement following treatment. The variation trend of various nerve cells demonstrated a notable increase in the proportion of oligodendrocytes and oligodendrocyte precursor cells in the autism group, which subsequently exhibited a significant decline following treatment. Five hub genes (MBP, PLIP, CNP, GFAP, and TAOK1) were verified by qPCR. Finally, MR studies have confirmed a causal relationship between hippocampal myelination-related gene expression and the risk of autism.Conclusions: AVP could markedly enhance social interaction abilities in the autism rat model, possibly due to the significantly improved hippocampus oligodendrocytes development and myelination.","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"394"},"PeriodicalIF":3.3,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755908","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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CELF6 as an Oncogene in Colorectal Cancer: Targeting Stem-Cell-Like Properties Through Modulation of HOXA5 mRNA Stability. CELF6作为结直肠癌的致癌基因：通过调节HOXA5 mRNA稳定性靶向干细胞样特性

IF 3.3

Frontiers in bioscience (Landmark edition) Pub Date : 2024-11-21 DOI: 10.31083/j.fbl2911395

Zhiming Fu, Xiang Wang, Zhiju Chen, Baochun Wang, Weiwei Huang, Xin Liu

{"title":"CELF6 as an Oncogene in Colorectal Cancer: Targeting Stem-Cell-Like Properties Through Modulation of HOXA5 mRNA Stability.","authors":"Zhiming Fu, Xiang Wang, Zhiju Chen, Baochun Wang, Weiwei Huang, Xin Liu","doi":"10.31083/j.fbl2911395","DOIUrl":"https://doi.org/10.31083/j.fbl2911395","url":null,"abstract":"Background: Emerging evidence indicates the essential role of cancer stem cells (CSCs) in the development and progression of various cancers, including colorectal cancer (CRC). CELF6, a member of the cytosine-uridine-guanine-binding protein (CUG-BP), Elav-like family (CELF), has been reported to be downregulated in CRC tissues. This study aims to elucidate the role and underlying mechanisms of CELF6 in CRC progression.Methods: The expression levels and prognostic significance of CELF6, along with its association with homeobox A5 (HOXA5), were analyzed using University of Alabama at Birmingham Cancer Data Analysis Portal (UALCAN), PrognoScan, and Tumor Immune Estimation Resource (TIMER) databases. The expression of CELF6 was further assessed through quantitative real-time polymerase chain reaction (qRT-PCR), immunoblotting, and immunohistochemistry. Both in vitro and in vivo experiments were conducted to investigate the effects of CELF6 on CRC cell proliferation, stemness and tumorigenesis, and to elucidate the molecular mechanisms.Results: CELF6 was found to be downregulated in CRC and was associated with poor prognosis. Functional studies revealed that overexpression of CELF6 resulted in decreased CRC cell proliferation and stemness in vitro, reduced tumor growth in vivo, and induced G1 phase cell cycle arrest. Mechanistically, CELF6 regulated the expression of HOXA5 by modulating its mRNA stability. Furthermore, the knockdown of HOXA5 reversed the inhibitory effects of CELF6 on CRC cell proliferation and stemness, demonstrating that silencing HOXA5 counteracted the suppressive effects of CELF6.Conclusions: This study is the first to identify CELF6 as a suppressor of stemness and a modulator of CRC progression. These findings provide new insights into the role of CELF6 in CRC and highlight its potential as a novel therapeutic target.","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"395"},"PeriodicalIF":3.3,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Interplay of Reactive Oxygen Species (ROS) and Epigenetic Remodelling in Cardiovascular Diseases Pathogenesis: A Contemporary Perspective. 活性氧（ROS）与表观遗传重塑在心血管疾病发病机制中的相互作用：当代视角

IF 3.3

Frontiers in bioscience (Landmark edition) Pub Date : 2024-11-21 DOI: 10.31083/j.fbl2911398

Amin Al-Awar, Shafaat Hussain

{"title":"Interplay of Reactive Oxygen Species (ROS) and Epigenetic Remodelling in Cardiovascular Diseases Pathogenesis: A Contemporary Perspective.","authors":"Amin Al-Awar, Shafaat Hussain","doi":"10.31083/j.fbl2911398","DOIUrl":"10.31083/j.fbl2911398","url":null,"abstract":"Cardiovascular diseases (CVDs) continue to be the leading cause of mortality worldwide, necessitating the development of novel therapies. Despite therapeutic advancements, the underlying mechanisms remain elusive. Reactive oxygen species (ROS) show detrimental effects at high concentrations but act as essential signalling molecules at physiological levels, playing a critical role in the pathophysiology of CVD. However, the link between pathologically elevated ROS and CVDs pathogenesis remains poorly understood. Recent research has highlighted the remodelling of the epigenetic landscape as a crucial factor in CVD pathologies. Epigenetic changes encompass alterations in DNA methylation, post-translational histone modifications, adenosine triphosphate (ATP)-dependent chromatin modifications, and noncoding RNA transcripts. Unravelling the intricate link between ROS and epigenetic changes in CVD is challenging due to the complexity of epigenetic signals in gene regulation. This review aims to provide insights into the role of ROS in modulating the epigenetic landscape within the cardiovascular system. Understanding these interactions may offer novel therapeutic strategies for managing CVD by targeting ROS-induced epigenetic changes. It has been widely accepted that epigenetic modifications are established during development and remain fixed once the lineage-specific gene expression pattern is achieved. However, emerging evidence has unveiled its remarkable dynamism. Consequently, it is now increasingly recognized that epigenetic modifications may serve as a crucial link between ROS and the underlying mechanisms implicated in CVD.","PeriodicalId":73069,"journal":{"name":"Frontiers in bioscience (Landmark edition)","volume":"29 11","pages":"398"},"PeriodicalIF":3.3,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142755956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0