Advanced biology最新文献_第7页

COL12A1 rs970547 Polymorphism Predisposes Anterior Cruciate Ligament Injury by Inducing ER Stress and Impairing Fibroblast Function. COL12A1 rs970547多态性通过诱导内质网应激和损害成纤维细胞功能而易导致前交叉韧带损伤。

IF 3.2 3区生物学

Advanced biology Pub Date : 2026-05-01 DOI: 10.1002/adbi.202500655

Wenchuan Zhao, Hong Chen, Junwei Wang, Yixin Li, Rui Chen, Jingyi Zhou

引用次数: 0

From Spider Webs to Brains: Can the Bri2 BRICHOS Molecular Chaperone Domain Transport Biological Drugs Into the Central Nervous System? 从蜘蛛网到大脑：Bri2 BRICHOS分子伴侣结构域能否将生物药物转运到中枢神经系统？

IF 3.2 3区生物学

Advanced biology Pub Date : 2026-05-01 DOI: 10.1002/adbi.202500721

Cloé Moëlo, Nina Kronqvist, Jan Johansson

{"title":"From Spider Webs to Brains: Can the Bri2 BRICHOS Molecular Chaperone Domain Transport Biological Drugs Into the Central Nervous System?","authors":"Cloé Moëlo, Nina Kronqvist, Jan Johansson","doi":"10.1002/adbi.202500721","DOIUrl":"10.1002/adbi.202500721","url":null,"abstract":"Biological drugs like antibodies or enzymes have very limited access to the central nervous system (CNS) because the blood-brain barrier (BBB) excludes macromolecules that are not required for brain homeostasis. To overcome this hurdle, different types of shuttle systems have been designed, such as linking the drugs to binders to transporters present in the BBB, thereby allowing receptor-meditated transcytosis (RMT), or encapsulating them in liposomes that have been modified to promote RMT and/or adsorptive-mediated transcytosis. These shuttles have given encouraging results but are at the same time associated with potential drawbacks like risk of interfering with transport of the endogenous ligands, immune responses and limited efficiencies to deliver the cargo drugs further to intracellular targets. BRICHOS is a 14 kDa protein domain present in ten human protein families and apparently specialised to prevent amyloid toxicity. Recent studies have shown that recombinant BRICHOS from the Bri2 protein can be used to transcytose model cargo protein from spider silk over vascular endothelial cells and promote endocytosis into neurons in the CNS of mice. Here, the potential of harnessing recombinant Bri2 BRICHOS for the transport of biological drugs into the CNS parenchyma and cells is discussed.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 5","pages":"e00721"},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147961821","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

miR-210 in Ischemic Cardiovascular Disease: Functions, Mechanisms, and Therapeutic Potential. miR-210在缺血性心血管疾病中的作用、机制和治疗潜力

IF 3.2 3区生物学

Advanced biology Pub Date : 2026-05-01 DOI: 10.1002/adbi.202500653

Wanqiu Zhang, Kexin Zhang, Yujie Ma, Zhenghui Tian, Chengxia Kan, Jingwen Zhang, Xiaodong Sun

{"title":"miR-210 in Ischemic Cardiovascular Disease: Functions, Mechanisms, and Therapeutic Potential.","authors":"Wanqiu Zhang, Kexin Zhang, Yujie Ma, Zhenghui Tian, Chengxia Kan, Jingwen Zhang, Xiaodong Sun","doi":"10.1002/adbi.202500653","DOIUrl":"10.1002/adbi.202500653","url":null,"abstract":"Ischemic cardiovascular disease remains a leading cause of morbidity and mortality worldwide despite advances in pharmacological, interventional, and rehabilitative therapies. Hypoxia-inducible microRNA-210 (miR-210) has emerged as a central mediator of cellular adaptation to oxygen deprivation and ischemic injury. As a prototypical \"hypoxamir,\" miR-210 regulates metabolic reprogramming, apoptosis, angiogenesis, and vascular remodeling, thereby influencing disease onset, progression, and repair. Its expression is governed by transcription factors, while downstream targets modulate mitochondrial function, DNA repair, and apoptotic signaling. Functionally, miR-210 enhances cardiomyocyte survival, promotes endothelial migration and tube formation, attenuates fibrosis, and supports stem cell adaptation. Clinical studies reveal that circulating and exosomal miR-210 correlate with infarct size, collateral formation, and prognosis, suggesting biomarker potential. Preclinical evidence further highlights therapeutic applications through mimics, antagomirs, nanoparticles, and stem cell-derived exosomes, though delivery and safety challenges remain. This review aims to synthesize current knowledge on the regulatory network and functional roles of miR-210 in ischemic cardiovascular disease, and to evaluate its prospects as both a biomarker and a therapeutic target.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 5","pages":"e00653"},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147961770","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

Copper Overload Affects α-Synuclein Clearance Mechanisms in a Parkinson's Disease In Vitro Model. 铜超载影响帕金森病体外模型中α-突触核蛋白清除机制

IF 3.2 3区生物学

Advanced biology Pub Date : 2026-05-01 DOI: 10.1002/adbi.202500274

Debora Musarò, Marina Damato, Chiara Coppola, Marco Greco, Michele Maffia

{"title":"Copper Overload Affects α-Synuclein Clearance Mechanisms in a Parkinson's Disease In Vitro Model.","authors":"Debora Musarò, Marina Damato, Chiara Coppola, Marco Greco, Michele Maffia","doi":"10.1002/adbi.202500274","DOIUrl":"10.1002/adbi.202500274","url":null,"abstract":"Parkinson's disease (PD) is a common neurodegenerative disorder characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta and the formation of Lewy bodies, abnormal protein aggregates primarily composed of α-synuclein. Copper, an essential trace element, plays a role in α-synuclein aggregation and PD pathogenesis. This study examines the effects of copper overload on α-synuclein clearance pathways, focusing on autophagy and the ubiquitin-proteasome system (UPS) in dopaminergic SH-SY5Y neuroblastoma cells. Copper exposure enhances autophagosome formation, as indicated by increased Beclin-1 and LC3-II levels, and impairs autophagic flux, evidenced by LC3-II accumulation in the presence of chloroquine. Concurrently, copper increases polyubiquitinated proteins, suggesting UPS dysfunction, which is confirmed through MG132 treatment. These disruptions lead to the accumulation and aggregation of α-synuclein, particularly in its phosphorylated form. Immunofluorescence reveals neurite-localized α-synuclein aggregates, consistent with copper's role in α-synuclein pathology. This study highlights copper dyshomeostasis as a contributor to impaired α-synuclein clearance through autophagy and UPS dysfunction, advancing the understanding of PD's molecular basis.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 5","pages":"e00274"},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13136777/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809214","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

Cibotii Rhizoma Extract Mitigates LPS-Induced Inflammatory Bone Loss by Inhibiting the RANK Signaling Pathway to Suppress Osteoclastogenesis and Bone Resorption. 黄芪提取物通过抑制RANK信号通路抑制破骨细胞生成和骨吸收来减轻脂多糖诱导的炎症性骨丢失。

IF 3.2 3区生物学

Advanced biology Pub Date : 2026-05-01 DOI: 10.1002/adbi.202500599

Jin Young Hong, Wan-Jin Jeon, Hyunseong Kim, Junseon Lee, Hyun Kim, Changhwan Yeo, Yoon Jae Lee, In-Hyuk Ha

{"title":"Cibotii Rhizoma Extract Mitigates LPS-Induced Inflammatory Bone Loss by Inhibiting the RANK Signaling Pathway to Suppress Osteoclastogenesis and Bone Resorption.","authors":"Jin Young Hong, Wan-Jin Jeon, Hyunseong Kim, Junseon Lee, Hyun Kim, Changhwan Yeo, Yoon Jae Lee, In-Hyuk Ha","doi":"10.1002/adbi.202500599","DOIUrl":"10.1002/adbi.202500599","url":null,"abstract":"Bone homeostasis is maintained through balanced interactions between osteoblasts and osteoclasts, whereas chronic inflammation disrupts this balance by enhancing osteoclast activity and bone loss. This study investigated the protective effects of Cibotii Rhizoma (CR) on inflammatory bone destruction and its underlying mechanisms. In vitro, CR suppressed receptor activator of nuclear factor kappa B ligand (RANKL)-induced osteoclastogenesis in bone marrow-derived monocyte/macrophage (BMM) cultures by downregulating NFATc1, c-Src, and TRAF6, thereby inhibiting osteoclast formation, podosomal actin ring assembly, and cell fusion. In vivo, administration of CR in an LPS-induced bone loss mouse model preserved bone microarchitecture, as confirmed by micro-CT and histological analyses, and significantly reduced osteoclast numbers and calvarial bone erosion. Immunohistochemical staining further revealed decreased RANK and NFATc1 activity in calvarial bone tissue following CR treatment. Collectively, these findings indicate that CR mitigates inflammatory bone loss by targeting RANK signaling to inhibit osteoclastogenesis and bone resorption, highlighting its potential as a therapeutic agent for inflammatory bone diseases.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 5","pages":"e00599"},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809208","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

KAT6A Promotes Lung Cancer Proliferation and Invasion via Keap1-Nrf2 Signaling. KAT6A通过Keap1-Nrf2信号促进肺癌的增殖和侵袭。

IF 3.2 3区生物学

Advanced biology Pub Date : 2026-05-01 DOI: 10.1002/adbi.202500503

Qian Ning, Weichao Bai, Hong Li, Jing Xue, Dan Li, Tianjun Chen

{"title":"KAT6A Promotes Lung Cancer Proliferation and Invasion via Keap1-Nrf2 Signaling.","authors":"Qian Ning, Weichao Bai, Hong Li, Jing Xue, Dan Li, Tianjun Chen","doi":"10.1002/adbi.202500503","DOIUrl":"10.1002/adbi.202500503","url":null,"abstract":"This study aimed to investigate the role of lysine acetyltransferase 6A (KAT6A) in lung cancer progression and its potential involvement in Nrf2-related oxidative stress regulation. KAT6A was overexpressed or silenced in A549 and H1299 lung cancer cells. KAT6A expression was verified by quantitative reverse transcription polymerase chain reaction and Western blot. Cell Counting Kit-8 and Transwell assays showed that KAT6A overexpression promoted cell proliferation and invasion, whereas KAT6A silencing suppressed cell proliferation. KAT6A overexpression decreased the expression of Keap1 protein and enhanced Nrf2 signaling activity. Oxidative stress evaluation using 2',7'-dichlorodihydrofluorescein diacetate staining, malondialdehyde (MDA) detection, and superoxide dismutase (SOD) activity assays indicated decreased reactive oxygen species levels, reduced MDA content, and elevated SOD activity. Co-immunoprecipitation confirmed the interaction between KAT6A and Nrf2, and dual-luciferase reporter assays showed enhanced Nrf2 transcriptional activity on the heme oxygenase-1 promoter. Silencing Nrf2 reversed the effects of KAT6A on proliferation. Immunohistochemistry of clinical lung adenocarcinoma samples showed that high KAT6A expression correlated with advanced tumor stage and shorter overall survival. These findings suggest that KAT6A regulates oxidative stress via the Keap1-Nrf2 pathway, thereby promoting malignant progression in lung adenocarcinoma, and may serve as a potential prognostic biomarker.","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 5","pages":"e00503"},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147809262","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

Mir-301b-3p Targets Alx4 to Suppress Cisplatin Sensitivity in Breast Cancer through DNA Damage Mir-301b-3p通过DNA损伤靶向Alx4抑制乳腺癌顺铂敏感性

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-04-07 DOI: 10.1002/adbi.202500715

Yan Yan, Jianhong Xia, Tingting Ma, Liqing Zhou

{"title":"Mir-301b-3p Targets Alx4 to Suppress Cisplatin Sensitivity in Breast Cancer through DNA Damage","authors":"Yan Yan, Jianhong Xia, Tingting Ma, Liqing Zhou","doi":"10.1002/adbi.202500715","DOIUrl":"10.1002/adbi.202500715","url":null,"abstract":"<div>\u0000 \u0000 Objective: To elucidate how ALX Homeobox 4 (ALX4) modulates cisplatin sensitivity via DNA damage regulation in breast cancer (BC), this study explored the established role of mRNA-mediated DNA repair in driving chemoresistance. Methods: Integrated bioinformatics and molecular experiments identified ALX4 and miR-301b-3p expression patterns in BC cells. Potential binding sites between them were predicted and verified by dual-luciferase assays. Cellular experiments determined cisplatin IC50 via CCK-8 assays, while functional impacts of the miR-301b-3p/ALX4 axis on proliferation, apoptosis, and cisplatin-induced DNA damage were assessed using CCK-8, flow cytometry, alkaline comet assays, and western blot. Results: Our study identified downregulated ALX4 and upregulated miR-301b-3p in BC tissues. miR-301b-3p directly targeted ALX4, as confirmed by dual-luciferase assays. Overexpression of ALX4 inhibited BC cell proliferation, promoted apoptosis, enhanced cisplatin-induced DNA damage, and increased cisplatin sensitivity. Conversely, miR-301b-3p negatively regulated ALX4, thereby modulating DNA damage and cellular response to cisplatin. Conclusion: This study demonstrates that miR-301b-3p promotes BC proliferation and reduces cisplatin sensitivity by suppressing ALX4, a mechanism mediated through the regulation of DNA damage pathways. These findings offer new insights into cisplatin resistance and suggest potential therapeutic targets for overcoming chemoresistance in BC.\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 4","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147626458","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

Burden, Trends and Prediction of NAFLD/MAFLD Attributable to Smoking From 1990 to 2021: GBD 2021 Analysis 1990 - 2021年吸烟所致NAFLD/MAFLD的负担、趋势和预测：GBD 2021分析

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-03-31 DOI: 10.1002/adbi.202500232

Lijuan Chen, Ziyi Zhu, Yishu Wang, Lin Guo, Zhenzhen Fu, Xianyong Yin, John Zhong Li, Yingyun Gong, Hongwen Zhou

{"title":"Burden, Trends and Prediction of NAFLD/MAFLD Attributable to Smoking From 1990 to 2021: GBD 2021 Analysis","authors":"Lijuan Chen, Ziyi Zhu, Yishu Wang, Lin Guo, Zhenzhen Fu, Xianyong Yin, John Zhong Li, Yingyun Gong, Hongwen Zhou","doi":"10.1002/adbi.202500232","DOIUrl":"10.1002/adbi.202500232","url":null,"abstract":"<div>\u0000 \u0000 Smoking is a risk factor for non-alcoholic fatty liver disease (NAFLD, recently proposed as metabolic dysfunction‑associated fatty liver disease, MAFLD), but the global smoking-attributable NAFLD/MAFLD burden remains unclear. Using GBD 2021 data, this study quantified the burden by age, sex, socio-demographic index (SDI), and region, computed average annual percent changes (AAPC) via Joinpoint regression, and projected 2022–2036 burden using the Bayesian age-period-cohort (BAPC) model. During 1990–2021, the AAPC of the age-standardized DALY rate (ASDR) and mortality rate (ASMR) was 0.0223 [95% uncertainty interval (UI): −0.1432, 0.1880, p = 0.79] and 0.2660 (95%UI: 0.1666, 0.3655, p < 0.001), suggesting that the death-related burden increased mostly. Notably, males contributed the most to this trend, with the sharpest upward trend recorded in low-middle SDI regions. Global cross-country inequality revealed that this death-related burden is widening, especially among females. In contrast to this historical trajectory, predictive models suggest a steady decline by 2036. In conclusion, global ASMR of smoking-attributable NAFLD/MAFLD increased during 1990–2021, especially in low-middle SDI regions and male populations. Despite a projected gradual burden decline over the next 15 years, it still emphasizes the need for strengthened tobacco control and NAFLD/MAFLD prevention in low-middle SDI regions and male populations.\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 4","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147589135","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

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-03-24

引用次数: 0

Transcriptional Activation of SBNO2 by KDM1A Drives Immune Escape in Lung Cancer KDM1A转录激活SBNO2驱动肺癌免疫逃逸

IF 2.6 3区生物学

Advanced biology Pub Date : 2026-03-24 DOI: 10.1002/adbi.202500639

Deguang Pan, Chong Zhang

{"title":"Transcriptional Activation of SBNO2 by KDM1A Drives Immune Escape in Lung Cancer","authors":"Deguang Pan, Chong Zhang","doi":"10.1002/adbi.202500639","DOIUrl":"10.1002/adbi.202500639","url":null,"abstract":"<div>\u0000 \u0000 KDM1A is a crucial epigenetic modulator in tumor immune escape. Nevertheless, its precise regulatory function within the immune microenvironment of lung cancer needs investigation. Using TCGA data, we analyzed KDM1A and SBNO2 expression, clinical correlation, and immune infiltration. Functional assays included co-culture of lung cancer cells with CD8+ T cells, flow cytometry, Transwell migration, ChIP, and luciferase reporter assays. qPCR measured gene expression. KDM1A and SBNO2 were notably upregulated in lung cancer tissues, which correlated with poor patient prognosis and reduced CD8+ T cell infiltration. Functional experiments demonstrated that knockdown of KDM1A enhanced T cell proliferation, chemotaxis, and cytokine production. Mechanistically, KDM1A acted as a transcription regulator binding to the SBNO2 promoter and positively regulated its mRNA expression in lung cancer cells. Importantly, rescue experiments confirmed that silencing SBNO2 expression abolished the pro-tumor immune escape effects induced by KDM1A overexpression. This study unveils a novel mechanism whereby KDM1A drives immune escape in lung cancer by transcriptionally activating SBNO2, which subsequently suppresses the anti-tumor role of CD8+ T cells. These findings lend strong support to targeting the KDM1A-SBNO2 axis as a promising immunotherapeutic approach for lung cancer.\u0000 </div>","PeriodicalId":7234,"journal":{"name":"Advanced biology","volume":"10 3","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147502820","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