BioEssays最新文献_第3页

Issue Information: BioEssays 2/2025

IF 3.2 3区生物学

BioEssays Pub Date : 2025-01-23 DOI: 10.1002/bies.202570002

引用次数: 0

Assessing Human Ribosomal DNA Variation and Its Association With Phenotypic Outcomes 评估人类核糖体DNA变异及其与表型结果的关系。

IF 3.2 3区生物学

BioEssays Pub Date : 2025-01-20 DOI: 10.1002/bies.202400232

Francisco Rodriguez-Algarra, Elliott Whittaker, Sandra del Castillo del Rio, Vardhman K. Rakyan

{"title":"Assessing Human Ribosomal DNA Variation and Its Association With Phenotypic Outcomes","authors":"Francisco Rodriguez-Algarra, Elliott Whittaker, Sandra del Castillo del Rio, Vardhman K. Rakyan","doi":"10.1002/bies.202400232","DOIUrl":"10.1002/bies.202400232","url":null,"abstract":"<p>Although genome-scale analyses have provided insights into the connection between genetic variability and complex human phenotypes, much trait variation is still not fully understood. Genetic variation within repetitive elements, such as the multi-copy, multi-locus ribosomal DNA (rDNA), has emerged as a potential contributor to trait variation. Whereas rDNA was long believed to be largely uniform within a species, recent studies have revealed substantial variability in the locus, both within and across individuals. This variation, which takes the form of copy number, structural arrangement, and sequence differences, has been found to be associated with human phenotypes. This review summarizes what is currently known about human rDNA variation, its causes, and its association with phenotypic outcomes, highlighting the technical challenges the field faces and the solutions proposed to address them. Finally, we suggest experimental approaches that can help clarify the elusive mechanisms underlying the phenotypic consequences of rDNA variation.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 4","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.202400232","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000411","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}

引用次数: 0

Mechanisms of Lipid-Associated Macrophage Accrual in Metabolically Stressed Adipose Tissue 代谢应激脂肪组织中脂质相关巨噬细胞积累的机制。

IF 3.2 3区生物学

BioEssays Pub Date : 2025-01-19 DOI: 10.1002/bies.202400203

Isabel Reinisch, Sarah Enzenhofer, Andreas Prokesch

{"title":"Mechanisms of Lipid-Associated Macrophage Accrual in Metabolically Stressed Adipose Tissue","authors":"Isabel Reinisch, Sarah Enzenhofer, Andreas Prokesch","doi":"10.1002/bies.202400203","DOIUrl":"10.1002/bies.202400203","url":null,"abstract":"<p>Adipose tissue (AT) inflammation, a hallmark of the metabolic syndrome, is triggered by overburdened adipocytes sending out immune cell recruitment signals during obesity development. An AT immune landscape persistent throughout weight loss and regain constitutes an immune-obesogenic memory that hinders long-term weight loss management. Lipid-associated macrophages (LAMs) are emerging as major players in diseased, inflamed metabolic tissues and may be key contributors to an obesogenic memory in AT. Our previous study found that LAM abundance increases with weight loss via intermittent fasting (IF) in obese mice, which is driven by adipocyte p53 signalling. However, the specific signals causing LAM accumulation in AT under IF remain unknown. In this piece, we hypothesise on a range of adipocyte-secreted signals that can harbor immune-attractive features upon fasting/refeeding cycles. We highlight possible mechanisms including cell death signalling, matrikines, and other damage-associated molecular patterns (DAMPs), as well as adipo(-cyto)kines, lipid mediators, metabolites, extracellular vesicles, and epigenetic rewiring. Finally, we consider how advances in mechanisms of AT LAM recruitment gleaned from preclinical models might be translatable to long-term weight management in humans. Thus, we provide vantage points to study signals driving monocyte recruitment, polarisation towards LAMs, and LAM retention, to harness the therapeutic potential of modulating AT LAM levels by impacting the immune-obesogenic memory in metabolic disease.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 4","pages":""},"PeriodicalIF":3.2,"publicationDate":"2025-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.202400203","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000413","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}

引用次数: 0

Nucleic Acid Aptamer-Based Sensors for Bacteria Detection: A Review 基于核酸适体的细菌检测传感器研究进展

IF 3.2 3区生物学

BioEssays Pub Date : 2025-01-16 DOI: 10.1002/bies.202400111

Yalan Tang, Yun Li, Ping Chen, Shian Zhong, Yanjing Yang

引用次数: 0

Metabolic Dysregulation as a Central Mechanism in 16p11.2 Deletion Syndrome: A Multigenic Perspective on Clinical Variability and Therapeutic Opportunities 代谢失调是16p11.2缺失综合征的中心机制：临床变异性和治疗机会的多基因视角

IF 3.2 3区生物学

BioEssays Pub Date : 2025-01-15 DOI: 10.1002/bies.202400299

Rana Fetit

引用次数: 0

Epithelial Polarity Loss and Multilayer Formation: Insights Into Tumor Growth and Regulatory Mechanisms 上皮极性丧失和多层形成：对肿瘤生长和调节机制的见解。

IF 3.2 3区生物学

BioEssays Pub Date : 2024-12-31 DOI: 10.1002/bies.202400189

Jie Sun, Md Biplob Hosen, Wu-Min Deng, Aiguo Tian

{"title":"Epithelial Polarity Loss and Multilayer Formation: Insights Into Tumor Growth and Regulatory Mechanisms","authors":"Jie Sun, Md Biplob Hosen, Wu-Min Deng, Aiguo Tian","doi":"10.1002/bies.202400189","DOIUrl":"10.1002/bies.202400189","url":null,"abstract":"<div>\u0000 \u0000 <p>Epithelial tissues serve as critical barriers in metazoan organisms, maintaining structural integrity and facilitating essential physiological functions. Epithelial cell polarity regulates mechanical properties, signaling, and transport, ensuring tissue organization and homeostasis. However, the barrier function is challenged by cell turnover during development and maintenance. To preserve tissue integrity while removing dying or unwanted cells, epithelial tissues employ cell extrusion. This process removes both dead and live cells from the epithelial layer, typically causing detached cells to undergo apoptosis. Transformed cells, however, often resist apoptosis, leading to multilayered structures and early carcinogenesis. Malignant cells may invade neighboring tissues. Loss of cell polarity can lead to multilayer formation, cell extrusion, and invasion. Recent studies indicate that multilayer formation in epithelial cells with polarity loss involves a mixture of wild-type and mutant cells, leading to apical or basal accumulation. The directionality of accumulation is regulated by mutations in polarity complex genes. This phenomenon, distinct from traditional apical or basal extrusion, exhibits similarities to the endophytic or exophytic growth observed in human tumors. This review explores the regulation and implications of these phenomena for tissue biology and disease pathology.</p>\u0000 </div>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 3","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142906623","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Vascular-Associated Mononuclear Phagocytes: First-Line Soldiers Ambushing Metastasis

IF 3.2 3区生物学

BioEssays Pub Date : 2024-12-29 DOI: 10.1002/bies.202400261

Han-ying Huang, Xin-nan Zheng, Lin Tian

{"title":"Vascular-Associated Mononuclear Phagocytes: First-Line Soldiers Ambushing Metastasis","authors":"Han-ying Huang, Xin-nan Zheng, Lin Tian","doi":"10.1002/bies.202400261","DOIUrl":"https://doi.org/10.1002/bies.202400261","url":null,"abstract":"<div>\u0000 \u0000 <p>Mononuclear phagocytes (MPs), which consist of dendritic cells, monocytes, and macrophages, are distributed throughout the body and actively eliminate invading microorganisms and abnormal cells. Depending on the local microenvironment, MPs manifest considerably various lifespans and phenotypes to maintain tissue homeostasis. Vascular-associated mononuclear phagocytes (VaMPs) are the special subsets of MPs that are localized either within the lumen side or on the apical surface of vessels, acting as the critical sentinels to recognize and defend against disseminated tumor cells. In this review, we introduce three major types of VaMPs, patrolling monocytes, Kupffer cells, and perivascular macrophages, and discuss their emerging roles in immunosurveillance during incipient metastasis. We also explore the roles of lineage-determining transcription factors and cell surface receptors that endow VaMPs with potent anti-tumor activity. Finally, we highlight the molecular and cellular mechanisms that drive the phenotypic plasticity of VaMPs and summarize combinatory strategies for targeting VaMPs in overt metastasis.</p>\u0000 </div>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 3","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143475849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A Hypothesis: Metabolic Contributions to 16p11.2 Deletion Syndrome 一个假设代谢对 16p11.2 缺失综合征的影响

IF 3.2 3区生物学

BioEssays Pub Date : 2024-12-29 DOI: 10.1002/bies.202400177

Brandon Kar Meng Choo, Sarah Barnes, Hazel Sive

引用次数: 0

New Horizons in Myotonic Dystrophy Type 1: Cellular Senescence as a Therapeutic Target 1型强直性肌营养不良的新视野：细胞衰老作为治疗靶点。

IF 3.2 3区生物学

BioEssays Pub Date : 2024-12-26 DOI: 10.1002/bies.202400216

Cécilia Légaré, J. Andrew Berglund, Elise Duchesne, Nicolas A. Dumont

{"title":"New Horizons in Myotonic Dystrophy Type 1: Cellular Senescence as a Therapeutic Target","authors":"Cécilia Légaré, J. Andrew Berglund, Elise Duchesne, Nicolas A. Dumont","doi":"10.1002/bies.202400216","DOIUrl":"10.1002/bies.202400216","url":null,"abstract":"<p>Myotonic dystrophy type 1 (DM1) is considered a progeroid disease (i.e., causing premature aging). This hypervariable disease affects multiple systems, such as the musculoskeletal, central nervous, gastrointestinal, and others. Despite advances in understanding the underlying pathogenic mechanism of DM1, numerous gaps persist in our understanding, hindering elucidation of the heterogeneity and severity of its symptoms. Accumulating evidence indicates that the toxic intracellular RNA accumulation associated with DM1 triggers cellular senescence. These cells are in a state of irreversible cell cycle arrest and secrete a cocktail of cytokines, referred to as a senescence-associated secretory phenotype (SASP), that can have harmful effects on neighboring cells and more broadly. We hypothesize that cellular senescence contributes to the pathophysiology of DM1, and clearance of senescent cells is a promising therapeutic approach for DM1. We will discuss the therapeutic potential of different senotherapeutic drugs, especially senolytics that eliminate senescent cells, and senomorphics that reduce SASP expression.</p>","PeriodicalId":9264,"journal":{"name":"BioEssays","volume":"47 3","pages":""},"PeriodicalIF":3.2,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/bies.202400216","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892431","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}

引用次数: 0

Neuropeptides: The Evergreen Jack-of-All-Trades in Neuronal Circuit Development and Regulation 神经肽：神经元回路发育和调控的常青树万能钥匙。

IF 3.2 3区生物学

BioEssays Pub Date : 2024-12-26 DOI: 10.1002/bies.202400238

Zsofia Hevesi, Tomas Hökfelt, Tibor Harkany

引用次数: 0