BMB Reports最新文献_第7页

Corin inhibits microglial inflammatory activation by suppressing mitochondrial dysfunction in intracerebral hemorrhage. Corin通过抑制脑出血线粒体功能障碍抑制小胶质细胞炎症激活。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-02-01

Rui Yin, Caixia Qiu, Qikai Shen, Zhong Wang

{"title":"Corin inhibits microglial inflammatory activation by suppressing mitochondrial dysfunction in intracerebral hemorrhage.","authors":"Rui Yin, Caixia Qiu, Qikai Shen, Zhong Wang","doi":"","DOIUrl":"","url":null,"abstract":"Microglial activation driving neuroinflammation is a key factor in secondary brain injury after intracerebral hemorrhage (ICH); however, the regulatory mechanisms remain unknown. This study investigates how corin influences microglial inflammatory activation and its underlying mechanisms. Corin expression in rat ICH brain tissue was assessed at multiple time points. To assess corin's effect on neurological function and microglial inflammation, ICH rats and oxygen-glucose deprivation plus hemin (OGD/H)-stimulated HAPI microglia were treated with corin-encoding lentivirus. Neurobehavioral performance was evaluated using the Morris water maze (MWM). Microglial activation was assessed via Iba-1, iNOS, and Arg-1 expression, cytokine secretion, and migration assays. To determine whether AMPK mediates corin's effects, cells were co-treated with Compound C (an AMPK inhibitor) and corin lentivirus. Corin expression decreased in ICH rat brain tissue, reaching its lowest level on day 3 post-ICH. Corin overexpression protected against ICH-induced neuronal apoptosis and improved neurological deficits as confirmed by MWM. Moreover, corin overexpression reduced microglial activation and inflammation in both ICH rats and OGD/H-stimulated microglial cells, ameliorated mitochondrial dysfunction, and increased the p-AMPK/AMPK ratio. The protective effects of corin on cell migration, inflammation, and mitochondrial function were reversed by Compound C, indicating AMPK is a downstream mediator of corin. Targeting corin offers a promising therapeutic strategy for ICH by reducing neuroinflammation and mitochondrial damage through AMPK activation and modulation of microglial inflammatory phenotype polarization. [BMB Reports 2026; 59(2): 143-150].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"143-150"},"PeriodicalIF":4.1,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12936600/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145773329","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

Deep learning application for genomic data analysis. 基因组数据分析的深度学习应用。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-01-01

Chang Beom Jeong, Hyein Cho, Daechan Park

引用次数: 0

Imperfect repair in aging: senescent cells and the hepatic fibrotic niche. 衰老过程中的不完全修复：衰老细胞和肝纤维化生态位。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-01-01

Juyeon Kim, Minseong Kim, Chuna Kim

{"title":"Imperfect repair in aging: senescent cells and the hepatic fibrotic niche.","authors":"Juyeon Kim, Minseong Kim, Chuna Kim","doi":"","DOIUrl":"","url":null,"abstract":"Aging proceeds in a nonuniform spatiotemporal manner across tissues. While metabolic stress and chronic inflammation are implicated, the underlying mechanisms remain elusive. Here, we propose that imperfect wound healing-a failure of full resolution-creates and sustains pathological niches that drive progressive age-related dysfunction. Using the liver as a model system, we deconstruct this 'imperfect repair'. We posit that it is driven by a pro-fibrotic, non-resolving microenvironment sustained by complex crosstalk between functionally heterogeneous senescent cells and non-senescent scar-associated cell (SAC) populations (including macrophages, endothelial cells (ECs), and hepatic stellate cells (HSCs)). This pathological ecosystem is further shaped by the spatial context of hepatic zonation collapse, and the dysregulation of core signaling hubs, like WNT, Transforming Growth Factor (TGF)-β, and YAP and TAZ (YAP/TAZ). Viewing aging through the lens of imperfect repair provides a unifying framework linking senescence, inflammation, and fibrosis. This perspective shifts the therapeutic paradigm from targeting single senescent cells toward engineering the pathological niche itself, and redirects focus from end-stage disease, to the sub-clinical, spatial origins of tissue vulnerability. [BMB Reports 2026; 59(1): 13-26].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"13-26"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867169/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145773286","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

Genetic architecture of human aging and longevity: Insights from genome-wide association studies. 人类衰老和长寿的遗传结构：来自全基因组关联研究的见解。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-01-01

Dabin Yoon, Jungsoo Gim

{"title":"Genetic architecture of human aging and longevity: Insights from genome-wide association studies.","authors":"Dabin Yoon, Jungsoo Gim","doi":"","DOIUrl":"","url":null,"abstract":"Aging represents a fundamental evolutionary feature shared across all living organisms, intrinsically coupled with development and lifespan. It is orchestrated by a complex polygenic architecture involving numerous small-effect variants distributed across diverse biological pathways, giving rise to striking interindividual variation in aging trajectories and lifespan. Over the past decade and a half, genome-wide association studies (GWAS) have uncovered multiple loci associated with lifespan, healthspan, exceptional longevity, and aging, converging on key biological processes such as lipid metabolism, inflammation, insulin/IGF signaling, and DNA repair. These discoveries have illuminated conserved molecular networks underlying the regulation of aging and longevity. Nevertheless, the identified variants collectively account for only a modest fraction of heritability, underscoring that aging and longevity arise from the cumulative and coordinated actions of myriad common alleles within complex biological networks. In this minireview, we synthesize major genetic insights from GWAS of aging and longevity, delineate recurrent pathways and molecular themes, and discuss how these findings refine our understanding of the genomic foundations of lifespan variation. We further highlight outstanding challenges, including phenotypic heterogeneity, ancestry-specific effects, and the limited predictive power of current models, and propose conceptual directions for future research aimed at establishing a more comprehensive and mechanistic framework for the genetic architecture of human aging and healthy longevity. [BMB Reports 2026; 59(1): 2-12].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"2-12"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951115","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

Integrating Perspectives on Aging: From Mechanistic Causes to Therapeutic Interventions. 衰老的综合观点：从机械原因到治疗干预。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-01-01

Eun-Soo Kwon

{"title":"Integrating Perspectives on Aging: From Mechanistic Causes to Therapeutic Interventions.","authors":"Eun-Soo Kwon","doi":"","DOIUrl":"","url":null,"abstract":"Aging poses one of the most urgent biomedical challenges of the 21st century, increasing vulnerability to chronic diseases and limiting healthspan in aging populations. Recent advances in aging research are transforming our understanding of aging from an inevitable decline to a multidimensional and potentially modifiable biological process. This special issue presents five invited reviews that collectively illustrate the recent progress in aging research. These articles introduce emerging concepts that shed light on the fundamental causes of aging, including the genetic architecture underlying human aging, senescence-driven fibrotic scarring arising from imperfect tissue repair, and the progressive erosion of epigenetic information in the brain. They further highlight promising avenues for intervention-such as epigenetic rejuvenation, the bidirectional interplay between the aging gut microbiome and host physiology, and the emergence of precision geronutrition. By integrating genetic, molecular, cellular, microbial, and nutritional perspectives, this collection emphasizes a future where extending human healthspan is both realistic and scientifically attainable. [BMB Reports 2026; 59(1): 1-1].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"1"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867178/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951131","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

Aging and the microbiome: implications for health and disease. 衰老和微生物群：对健康和疾病的影响。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-01-01

WenTing Gao, Hye-Yeon Lee, Kyung-Jin Min

{"title":"Aging and the microbiome: implications for health and disease.","authors":"WenTing Gao, Hye-Yeon Lee, Kyung-Jin Min","doi":"","DOIUrl":"","url":null,"abstract":"The gut microbiota plays a fundamental role in maintaining host homeostasis, and the aging process profoundly influences its composition and function. Accumulating evidence suggests that alterations in the gut microbiota are not just a consequence of aging, but also an active driver of age-related physiological decline. In particular, age-dependent gut microbiota dysbiosis has emerged as a critical factor contributing to host aging and aging-related diseases. This review systematically summarizes alterations in the gut microbiota (e.g., reduced alpha diversity, depletion of beneficial commensals, and enrichment of pathobionts) during the aging process, and discusses the spatiotemporal dynamics and causal relationships between microbial aging and host aging. The regulatory mechanisms by which the gut microbiota influences aging-related diseases, such as metabolic disorders (e.g., obesity, type 2 diabetes, and cardiovascular disease), immunosenescence, and neurodegenerative diseases (e.g., Alzheimer's disease and Parkinson's disease), are also elucidated. Finally, microbiota-targeted intervention strategies (e.g., probiotics, prebiotics, and postbiotics) are explored, together with advanced research strategies. [BMB Reports 2026; 59(1): 40-50].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"40-50"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145585809","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

Cdk1-dependent lamin aggregation underlies oxidative stress-induced nuclear shape abnormalities. cdk1依赖性层粘连蛋白聚集是氧化应激诱导的核形状异常的基础。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-01-01

Ju-Hyun Ahn, Min-Guk Cho, Abdul Basit, In-Kang Song, Kong-Joo Lee, Jae-Ho Lee

{"title":"Cdk1-dependent lamin aggregation underlies oxidative stress-induced nuclear shape abnormalities.","authors":"Ju-Hyun Ahn, Min-Guk Cho, Abdul Basit, In-Kang Song, Kong-Joo Lee, Jae-Ho Lee","doi":"","DOIUrl":"","url":null,"abstract":"Altered nuclear morphology, one of the characteristics of cancer cells, is often indicative of tumor prognosis. While reactive oxygen species (ROS) are known to induce nuclear morphology changes, mechanisms underlying these effects remain elusive, particularly regarding nuclear assembly. We hypothesized that mitotic cells might exhibit increased susceptibility to ROSinduced nuclear deformation due to the dynamic nature of nuclear envelope during mitosis, i.e., disassembly and reassembly. Interestingly, we discovered that exposure of mitotic cells to hydrogen peroxide (H2O2) resulted in persistence of lamin aggregates during early mitosis, which coincided with aberrant nuclear morphology. Further investigation revealed a dampening effect of H2O2 on Cdk1, a pivotal kinase governing mitotic entry. Our in vitro kinase assays demonstrated that H2O2 mediated reduction of Cdk1 activity, resulting in diminished phosphorylation of lamin, a key Cdk1 substrate. Notably, restoration of Cdk1 activity rescued lamin phosphorylation, thereby mitigating lamin aggregation. Furthermore, persistence of lamin aggregation during mitotic entry correlated with premature reassembly of lamin during mitotic exit, affecting nuclear envelope reassembly. These findings collectively suggest that ROS-mediated perturbation of Cdk1 activity during early mitosis can trigger lamin aggregation that affects lamin reassembly, thereby disrupting nuclear morphology. Our study elucidates a novel mechanism by which ROS can disrupt nuclear architecture by modulating Cdk1 activity during mitosis. [BMB Reports 2026; 59(1): 69-77].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"69-77"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867170/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145013745","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

Epigenetic aging and rejuvenation of the brain: drivers, consequences, and interventions. 脑的表观遗传老化和再生：驱动因素、后果和干预。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-01-01

Seunghyun Lee, SeungA Cho, Seung-Kyoon Kim, Jae-Hyun Yang

引用次数: 0

Lefty2 prevents RANKL-induced bone loss by inhibiting osteoclast differentiation. Lefty2通过抑制破骨细胞分化来阻止rankl诱导的骨质流失。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-01-01

Jung Ha Kim, Kabsun Kim, Inyoung Kim, Semun Seong, Nacksung Kim

引用次数: 0

Precision geronutrition: personalized nutritional strategies to extend healthy lifespan. 精准老年营养：延长健康寿命的个性化营养策略。

IF 4.1 3区生物学

BMB Reports Pub Date : 2026-01-01

So-Hyun Park, Chang Hwa Jung, Jiyun Ahn

{"title":"Precision geronutrition: personalized nutritional strategies to extend healthy lifespan.","authors":"So-Hyun Park, Chang Hwa Jung, Jiyun Ahn","doi":"","DOIUrl":"","url":null,"abstract":"Aging is a multifactorial and heterogeneous biological process, where chronological age alone does not accurately reflect an individual's functional or physiological state. The emerging discipline of precision geronutrition integrates the principles of geroscience with precision nutrition, aiming to delay the onset of age-related functional decline by modulating fundamental molecular mechanisms, such as nutrient-sensing pathways (mTOR, AMPK, and sirtuins), inflammaging, and oxidative stress. A major barrier to progress has been the absence of validated biomarkers that can quantify biological aging and assess intervention efficacy. Recent advances in biological aging clocks, in particular DNA methylation-based epigenetic clocks, provide powerful tools to objectively measure biological age, and evaluate the impact of nutritional interventions. This review discusses how personalized dietary strategies, guided by multi-omics data (genomic, metabolomic, and microbiome profiles), can decelerate aging trajectories. We propose that individualized daily nutrition, aligned with an individual's unique biological characteristics, represents a targeted and actionable approach to extend healthspan. The integration of dynamic aging clocks into nutritional intervention frameworks will be essential to transition from a diseaseoriented model to a preventive, healthspan-centered paradigm. Future challenges include large-scale clinical validation, standardization of aging biomarkers, cost reduction, and translation into public health and clinical applications. [BMB Reports 2026; 59(1): 51-59].","PeriodicalId":9010,"journal":{"name":"BMB Reports","volume":" ","pages":"51-59"},"PeriodicalIF":4.1,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12867180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145773340","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