Advanced biology最新文献

Extracellular Vesicles in Aging and Age-Related Diseases. How Important Are They?

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-04-09 DOI: 10.1002/adbi.202400656

David J Lundy, Chia-Te Liao

{"title":"Extracellular Vesicles in Aging and Age-Related Diseases. How Important Are They?","authors":"David J Lundy, Chia-Te Liao","doi":"10.1002/adbi.202400656","DOIUrl":"https://doi.org/10.1002/adbi.202400656","url":null,"abstract":"Extracellular vesicles (EVs), lipid bilayer-bound particles secreted by cells, have attracted significant research attention for their roles in aging-related disorders, including cardiovascular disease, metabolic dysfunction, cancer, and neurodegeneration. Research shows that EV cargo and function are influenced by factors including age, disease state, exercise, nutrition and sleep, and they may modulate various aging-associated processes such as stem cell renewal, nutrient sensing, cell senescence, mitochondrial function, and insulin resistance. This perspective highlights, for a general audience, a selection of studies of EVs in aging and age-related diseases, and their diverse roles in organ crosstalk. While current evidence indicates that EVs play multiple roles in aging, there are numerous challenges including methodological challenges and limitations, heterogeneous reports of EV cargo, limited reproducibility, and apparent context-dependent effects of EVs and their cargo. Together, this limits the interpretation of these studies. This is proposed that EVs may act as fine-tuners of cellular communication within the broader aging-associated secretome and the importance of standardizing methods are emphasized. Last, future directions for EV research are suggested.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400656"},"PeriodicalIF":3.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810248","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

The Regulation of Trace Metal Elements in Cancer Ferroptosis.

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-04-09 DOI: 10.1002/adbi.202400821

Xiaoyan Wang, Yuanyuan Xue, Lei Chang, Xuena Zhu, Wenjun Liu, Tingbo Liang

{"title":"The Regulation of Trace Metal Elements in Cancer Ferroptosis.","authors":"Xiaoyan Wang, Yuanyuan Xue, Lei Chang, Xuena Zhu, Wenjun Liu, Tingbo Liang","doi":"10.1002/adbi.202400821","DOIUrl":"https://doi.org/10.1002/adbi.202400821","url":null,"abstract":"Ferroptosis, as novel type of regulated cell death that has garnered widespread attention over the past decade, has witnessed the continuous discovery of an increasing number of regulatory mechanisms. Trace metal elements play a multifaceted and crucial role in oncology. Interestingly, it has been increasingly evident that these elements, such as copper, are involved in the regulation of iron accumulation, lipid peroxidation and antiferroptotic systems, suggesting the existence of \"nonferrous\" mechanisms in ferroptosis. In this review, a comprehensive overview of the composition and mechanism of ferroptosis is provided. The interaction between copper metabolism (including cuproptosis) and ferroptosis in cancer, as well as the roles of other trace metal elements (such as zinc, manganese, cobalt, and molybdenum) in ferroptosis are specifically focused. Furthermore, the applications of nanomaterials based on these metals in cancer therapy are also reviewed and potential strategies for co-targeting ferroptosis and cuproptosis are explored. Nevertheless, in light of the intricate and ambiguous nature of these interactions, ongoing research is essential to further elucidate the \"nonferrous\" mechanisms of ferroptosis, thereby facilitating the development of novel therapeutic targets and approaches for cancer treatment.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400821"},"PeriodicalIF":3.2,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810260","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

Emerging Roles of Plant-Derived Extracellular Vesicles in Biotherapeutics: Advances, Applications, and Future Perspectives.

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-04-08 DOI: 10.1002/adbi.202500008

Cheng Li, Aoqiong Zeng, Li Li, Wei Zhao

引用次数: 0

Nanomaterials-Based Drug Delivery Systems for Therapeutic Applications in Osteoporosis.

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-04-08 DOI: 10.1002/adbi.202400721

Donghong Shi, Yuling Li, Meng Tian, Mengge Xue, Jinping Wang, Hailong An

{"title":"Nanomaterials-Based Drug Delivery Systems for Therapeutic Applications in Osteoporosis.","authors":"Donghong Shi, Yuling Li, Meng Tian, Mengge Xue, Jinping Wang, Hailong An","doi":"10.1002/adbi.202400721","DOIUrl":"https://doi.org/10.1002/adbi.202400721","url":null,"abstract":"The etiology of osteoporosis is rooted in the disruption of the intricate equilibrium between bone formation and bone resorption processes. Nevertheless, the conventional anti-osteoporotic medications and hormonal therapeutic regimens currently employed in clinical practice are associated with a multitude of adverse effects, thereby constraining their overall therapeutic efficacy and potential. Recently, nanomaterials have emerged as a promising alternative due to their minimal side effects, efficient drug delivery, and ability to enhance bone formation, aiding in restoring bone balance. This review delves into the fundamental principles of bone remodeling and the bone microenvironment, as well as current clinical treatment approaches for osteoporosis. It subsequently explores the research status of nanomaterial-based drug delivery systems for osteoporosis treatment, encompassing inorganic nanomaterials, organic nanomaterials, cell-mimicking carriers and exosomes mimics and emerging therapies targeting the osteoporosis microenvironment. Finally, the review discusses the potential of nanomedicine in treating osteoporosis and outlines the future trajectory of this burgeoning field. The aim is to provide a comprehensive reference for the application of nanomaterial-based drug delivery strategies in osteoporosis therapy, thereby fostering further advancements and innovations in this critical area of medical research.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400721"},"PeriodicalIF":3.2,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802136","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

Edaravone Alleviates BV-2 Microglia-Mediated Neuroinflammation Through the PI3K/AKT/ NF-κB Pathway.

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-04-08 DOI: 10.1002/adbi.202400501

Li Yang, Zhaoda Duan, Dongyao Xu, Yingqi Peng, Yuke Wu, Yujia Yang, Qian Yin, Lanxi Fang, Shan Yan, Chunyun Wu

{"title":"Edaravone Alleviates BV-2 Microglia-Mediated Neuroinflammation Through the PI3K/AKT/ NF-κB Pathway.","authors":"Li Yang, Zhaoda Duan, Dongyao Xu, Yingqi Peng, Yuke Wu, Yujia Yang, Qian Yin, Lanxi Fang, Shan Yan, Chunyun Wu","doi":"10.1002/adbi.202400501","DOIUrl":"https://doi.org/10.1002/adbi.202400501","url":null,"abstract":"Ischemic stroke (IS) poses a significant threat to human health. Research has demonstrated that microglia (MG)-mediated neuroinflammatory responses play a crucial role in the pathogenesis of IS. Consequently, inhibiting MG activation and reducing the inflammatory response may be key strategies for the clinical treatment of stroke and neurodegenerative diseases. Edaravone (EDA), a potent anti-inflammatory and antioxidant, is currently used in the clinical treatment of IS; however, its anti-inflammatory mechanisms remain inadequately understood. To address this, network pharmacology (NP) analysis is employed to identify the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway as a potential mediator of the inflammatory response triggered by activated microglia following EDA treatment. In vitro oxygen-glucose deprivation (OGD) is used to induce BV-2 MG activation, and an in vivo middle cerebral artery occlusion (MCAO) mouse model is established. Western blot and immunofluorescence staining are used to detect changes in the phosphorylation levels of pathway-related proteins and the expression of inflammatory factors. Additionally, the PI3K pathway inhibitor LY294002 and a PI3K overexpression plasmid are introduced to further analyze the expression changes of these markers. The results suggest that EDA may alleviate the inflammatory response mediated by activated MG through the PI3K/Akt signaling pathway.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400501"},"PeriodicalIF":3.2,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802100","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

Phytomolecule Epimedin C Mitigates Cartilage Extracellular Matrix Degradation and Osteoarthritis Progression in Rats.

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-04-08 DOI: 10.1002/adbi.202400685

Wenyao Yang, Xiangbo Meng, Jiming Li, Huijuan Cao, Ling Li, Cuishan Huang, Yingchao Wang, Wakam Chang, Sibylle Grad, Zhen Li, Ling Qin, Xinluan Wang

{"title":"Phytomolecule Epimedin C Mitigates Cartilage Extracellular Matrix Degradation and Osteoarthritis Progression in Rats.","authors":"Wenyao Yang, Xiangbo Meng, Jiming Li, Huijuan Cao, Ling Li, Cuishan Huang, Yingchao Wang, Wakam Chang, Sibylle Grad, Zhen Li, Ling Qin, Xinluan Wang","doi":"10.1002/adbi.202400685","DOIUrl":"https://doi.org/10.1002/adbi.202400685","url":null,"abstract":"Osteoarthritis (OA) is a common degenerative joint disease associated with chronic inflammation. Epimedin C (EpiC), flavonoid from Epimedin, enhances the extracellular matrix (ECM) expression in human chondrocytes in vitro. This study aims to investigate the effects of EpiC on osteoarthritis progress in vivo. OA is induced in Lewis rats by medial meniscus transection and treatment with intra-articular injections of EpiC. EpiC treatment reduces joint swelling and improves hindlimb weight distribution in MMT-induced OA rats. Pathological changes in cartilage are observed and evaluated by the osteoarthritis research society international (OARSI) score and both EpiC groups have lower OARSI scores than the OA group. The EpiC groups also exhibit higher positive expressions of collagen II and aggrecan, and lower MMP13 and ADAMTS5 in the cartilage. RNA-seq suggest that EpiC may attenuate MMT-induced ECM degradation by inhibiting the JAK-STAT pathway. EpiC promotes the gene expressions of Col2a1 and Acan, while inhibiting Mmp13 and Col10a1 in cartilage. EpiC reduces the phosphorylated STAT3 in human chondrocyte pellets stimulated with inflammatory cytokines. In conclusion, EpiC demonstrates potential as an OA therapeutic by reducing pain and ECM degradation through p-STAT3 inhibition.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400685"},"PeriodicalIF":3.2,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802141","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

Endurance Exercise Training Alleviates Hepatic Lipocalin-2 Release and Prevents Anxiety-Like Disorders in Chronically Stressed Mice.

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-04-08 DOI: 10.1002/adbi.202500015

Fengzhen Yang, Yajie Wang, Xiao Wang, Mei Wang, Kwok-Fai So, Lan Yan, Li Zhang

引用次数: 0

Electroacupuncture's Impact on the Hippocampal RAGE/LRP1 Receptor System in SAMP8 Mice.

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-04-08 DOI: 10.1002/adbi.202400377

Zhitao Hou, Jindi Ma, Xian Zhang, Liying Song, Yan Li, Xiaochen Song, Xinying Hu, Dongdong Li, Changyuan He, Yuefeng Sun, Hongbo Cai, Jing Chen

引用次数: 0

Activation of SIRT1 Reduces Renal Tubular Epithelial Cells Fibrosis in Hypoxia Through SIRT1-FoxO1-FoxO3-Autophagy Pathway.

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-04-08 DOI: 10.1002/adbi.202400583

Guangyu Wang, Lijuan Zhang, Jiaorong Tan, Fei Li, Yishan Jin, Limei He, Xin Yang

{"title":"Activation of SIRT1 Reduces Renal Tubular Epithelial Cells Fibrosis in Hypoxia Through SIRT1-FoxO1-FoxO3-Autophagy Pathway.","authors":"Guangyu Wang, Lijuan Zhang, Jiaorong Tan, Fei Li, Yishan Jin, Limei He, Xin Yang","doi":"10.1002/adbi.202400583","DOIUrl":"https://doi.org/10.1002/adbi.202400583","url":null,"abstract":"Heart failure-induced renal tubular epithelial cell fibrosis is an important pathological process that leads to chronic kidney disease. This study is to investigate the regulatory mechanism of over-expression or knock-down SIRT1 gene, alleviating hypoxia-induced HK2 cell fibrosis in heart failure. The focus is on the SIRT1-FoxO1-FoxO3-Autophagy pathway. In vitro experiments are performed by HK2cell line to simulate the normal oxygen state (Normoxia) and the hypoxia state (Hypoxia) caused by heart failure, SIRT1 gene over-expression by transfected vectors, knock-down and Rapamycin (RAPA)-induced cellular autophagy, and the cell models are divided into four subgroups, named control group, oeSIRT1, siSIRT1 and siSIRT1+RAPA. Western blotting (WB), real-time qPCR, immunofluorescence (IF), ELISA, and transmission electron microscopy are used to quantitatively or semi-quantitatively analyze the expression of FoxO1, FoxO3, SIRT1, Beclin1, LC-3, α-SMA, E- Cadherin, and collagen-I in cells or supernatants. It is demonstrated that activation of SIRT1 regulates the expression and activity of FoxO1 and FoxO3, thereby affecting autophagy. This modulation leads to a reduction in HK2 fibrosis markers (α-SMA and E-cadherin) and extracellular matrix deposition (collagen I), which ultimately attenuates renal tubular epithelial cell fibrosis. These findings provide new insights into potential therapeutic strategies for treating heart failure-induced renal tubular epithelial cell fibrosis by targeting the SIRT1-FoxO1-FoxO3-Autophagy pathway.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400583"},"PeriodicalIF":3.2,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802098","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

Toward Design Principles for Biomolecular Condensates for Metabolic Pathways.

IF 3.2 3区生物学

Advanced biology Pub Date : 2025-04-07 DOI: 10.1002/adbi.202400672

Alain A M André, Nikita Rehnberg, Ankush Garg, Magnus Kjærgaard

{"title":"Toward Design Principles for Biomolecular Condensates for Metabolic Pathways.","authors":"Alain A M André, Nikita Rehnberg, Ankush Garg, Magnus Kjærgaard","doi":"10.1002/adbi.202400672","DOIUrl":"https://doi.org/10.1002/adbi.202400672","url":null,"abstract":"Biology uses membrane-less organelles or biomolecular condensates as dynamic reaction compartments that can form or dissolve to regulate biochemical pathways. This has led to a flurry of research aiming to design new synthetic organelles that function as reaction crucibles for enzymes and biomolecular cascades in biotechnology. The mechanisms by which a condensate can enhance multistep biochemical processes including mass action, tuning the chemical environment, scaffolding and metabolic channelling is reviewed. These mechanisms are not inherently beneficial for the rate of enzymatic processes but can also inhibit a reaction. Similarly, some aspects of condensates are likely intrinsically inhibitory including retardation of diffusion, where the net effect of a condensate will be a trade-off between inhibitory and stimulatory effects. It is discussed which generalizable conclusions can be drawn so far and how close it is to design principles for condensates for enzyme cascades in microbial cell factories including which reactions are likely to be enhanced by condensates and which type of condensate will be suited for which reaction.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":" ","pages":"e2400672"},"PeriodicalIF":3.2,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802151","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