Life medicine最新文献_第4页

Regulatory cellular and molecular networks in the bone microenvironment during aging 衰老过程中骨骼微环境的细胞和分子调控网络

Life medicine Pub Date : 2024-05-02 DOI: 10.1093/lifemedi/lnae019

Lingli Zhang, Zhikun Wang, Yuan Zhang, Rui Ji, Zhiben Li, Jun Zou, Bo Gao

{"title":"Regulatory cellular and molecular networks in the bone microenvironment during aging","authors":"Lingli Zhang, Zhikun Wang, Yuan Zhang, Rui Ji, Zhiben Li, Jun Zou, Bo Gao","doi":"10.1093/lifemedi/lnae019","DOIUrl":"https://doi.org/10.1093/lifemedi/lnae019","url":null,"abstract":"\u0000 Age-induced abnormalities in bone metabolism disrupt the equilibrium between bone resorption and formation. This largely stems from disturbances in bone homeostasis, in which signaling pathways exert a significant regulatory influence. Aging compromises the functionality of the bone marrow mesenchymal stem cells (BMSCs), ultimately resulting in tissue dysfunction and pathological aging. Age-related bone degradation primarily manifests as reduced bone formation and the increased accumulation of bone marrow fat. Cellular senescence diminishes bone cell vitality, thereby disrupting the balance of bone remodeling. Intensive osteoclast differentiation leads to the generation of more osteoclasts and increased bone resorption. This review provides insight into the impact of aging on bone, encompassing bone cell states during the aging process and bone signaling pathway transformations. It primarily delves into aging-related signaling pathways, such as the bone morphogenetic protein/Smad, Wnt/β-catenin, osteoprotegerin/receptor activator of NF-κB ligand/receptor activator of NF-κB, connexin43/miR21, and nuclear factor erythroid 2-related factor 2/antioxidant response element pathways, seeking to enhance our comprehension of crucial bone cells and their secretory phenotypes during aging. Furthermore, the precise molecular regulatory mechanisms underlying the interactions between bone signaling pathways and aging are investigated.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"78 6","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141022093","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

Integration of single-cell transcriptome and chromatin accessibility and its application on tumor investigation.

Life medicine Pub Date : 2024-04-26 eCollection Date: 2024-04-01 DOI: 10.1093/lifemedi/lnae015

Chunyuan Yang, Yan Jin, Yuxin Yin

引用次数: 0

Mitochondrial transplantation for the treatment of cardiac and noncardiac diseases: mechanisms, prospective, and challenges.

Life medicine Pub Date : 2024-04-26 eCollection Date: 2024-04-01 DOI: 10.1093/lifemedi/lnae017

Xinyi Wang, Zhiyuan Liu, Ling Zhang, Guangyu Hu, Ling Tao, Fuyang Zhang

{"title":"Mitochondrial transplantation for the treatment of cardiac and noncardiac diseases: mechanisms, prospective, and challenges.","authors":"Xinyi Wang, Zhiyuan Liu, Ling Zhang, Guangyu Hu, Ling Tao, Fuyang Zhang","doi":"10.1093/lifemedi/lnae017","DOIUrl":"10.1093/lifemedi/lnae017","url":null,"abstract":"Mitochondrial transplantation (MT) is a promising therapeutic strategy that involves introducing healthy mitochondria into damaged tissues to restore cellular function. This approach has shown promise in treating cardiac diseases, such as ischemia-reperfusion injury, myocardial infarction, and heart failure, where mitochondrial dysfunction plays a crucial role. Transplanting healthy mitochondria into affected cardiac tissue has resulted in improved cardiac function, reduced infract size, and enhanced cell survival in preclinical studies. Beyond cardiac applications, MT is also being explored for its potential to address various noncardiac diseases, including stroke, infertility, and genetic mitochondrial disorders. Ongoing research focused on refining techniques for mitochondrial isolation, preservation, and targeted delivery is bolstering the prospects of MT as a clinical therapy. As the scientific community gains a deeper understanding of mitochondrial dynamics and pathology, the development of MT as a clinical therapy holds significant promise. This review provides an overview of recent research on MT and discusses the methodologies involved, including sources, isolation, delivery, internalization, and distribution of mitochondria. Additionally, it explores the effects of MT and potential mechanisms in cardiac diseases, as well as non-cardiac diseases. Future prospects for MT are also discussed.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"3 2","pages":"lnae017"},"PeriodicalIF":0.0,"publicationDate":"2024-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11749488/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054555","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bridging the organoid translational gap: integrating standardization and micropatterning for drug screening in clinical and pharmaceutical medicine.

Life medicine Pub Date : 2024-04-15 eCollection Date: 2024-04-01 DOI: 10.1093/lifemedi/lnae016

Haowei Yang, Jiawei Li, Zitian Wang, Davit Khutsishvili, Jiyuan Tang, Yu Zhu, Yongde Cai, Xiaoyong Dai, Shaohua Ma

{"title":"Bridging the organoid translational gap: integrating standardization and micropatterning for drug screening in clinical and pharmaceutical medicine.","authors":"Haowei Yang, Jiawei Li, Zitian Wang, Davit Khutsishvili, Jiyuan Tang, Yu Zhu, Yongde Cai, Xiaoyong Dai, Shaohua Ma","doi":"10.1093/lifemedi/lnae016","DOIUrl":"10.1093/lifemedi/lnae016","url":null,"abstract":"Synthetic organ models such as organoids and organ-on-a-chip have been receiving recognition from administrative agencies. Despite the proven success of organoids in predicting drug efficacy on laboratory scales, their translational advances have not fully satisfied the expectations for both clinical implementation and commercial applications. The transition from laboratory settings to clinical applications continues to encounter challenges. Employing engineering methodologies to facilitate the bridging of this gap for organoids represents one of the key directions for future advancement. The main measures to bridge the gap include environmental and phenotypic recapitulation, 3D patterning, matrix engineering, and multi-modality information acquisition and processing. Pilot whole-process clinical/pharmaceutical applications with fast and standardized organoid models will continuously offer convincing frontline optimization clues and driving forces to the organoid community, which is a promising path to translational organoid technologies.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"3 2","pages":"lnae016"},"PeriodicalIF":0.0,"publicationDate":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11748978/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Follicular fluid-derived exosomes rejuvenate ovarian aging through miR-320a-3p-mediated FOXQ1 inhibition 卵泡液源性外泌体通过 miR-320a-3p 介导的 FOXQ1 抑制作用使卵巢衰老恢复活力

Life medicine Pub Date : 2024-03-25 DOI: 10.1093/lifemedi/lnae013

Yu Liu, Hongbei Mu, Yu Chen, Kexin Li, Q. Mei, Lingjuan Wang, Tianyu Tang, Qiuzi Shen, Huaibiao Li, Ling Zhang, Jing Li, W. Xiang

{"title":"Follicular fluid-derived exosomes rejuvenate ovarian aging through miR-320a-3p-mediated FOXQ1 inhibition","authors":"Yu Liu, Hongbei Mu, Yu Chen, Kexin Li, Q. Mei, Lingjuan Wang, Tianyu Tang, Qiuzi Shen, Huaibiao Li, Ling Zhang, Jing Li, W. Xiang","doi":"10.1093/lifemedi/lnae013","DOIUrl":"https://doi.org/10.1093/lifemedi/lnae013","url":null,"abstract":"\u0000 Ovarian aging is mainly characterized by a progressive decline in oocyte quantity and quality, which ultimately leads to female infertility. Various therapies have been established to cope with ovarian aging, among which exosome-based therapy is considered a promising strategy that can benefit ovarian functions via multiple pathways. Here, we isolated and characterized exosomes derived from ovarian follicular fluid and profiled the differential expression patterns of noncoding exosomal RNAs in young and aged women. Treatment with young mouse-derived exosomes efficiently rescued ovarian function in aged mice. The follicular fluid exosomes from young mice and miR-320-3p can also promote the proliferation of ovarian granulosa cells and improve mitochondrial function from old mice in vitro. Exosomes can increase the number of primordial and growing follicles, and improve the developmental ability of oocytes in the old mice in vivo. The mechanism may be involve that exosomes transfer miR-320-3p to granulosa cells, and inhibit the expression of FOXQ1. And hnRNPA2B1 controls miR-320-3p entry into exosomes. This work provides insights into the antiaging potential of follicular fluid-derived exosomes and the underlying molecular mechanisms, which may facilitate prevention of ovarian aging and an improvement in female fertility.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":" 10","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140384410","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

Brain organoids: from unguided to regionalized to nucleus-specific 脑器质性组织：从无引导到区域化再到特异性细胞核

Life medicine Pub Date : 2024-03-22 DOI: 10.1093/lifemedi/lnae014

Yangfei Xiang, In-Hyun Park

引用次数: 0

Monkey multi-organ cell atlas exposed to estrogen.

Life medicine Pub Date : 2024-03-22 eCollection Date: 2024-04-01 DOI: 10.1093/lifemedi/lnae012

Wen Fang, Jiao Qu, Wanjun Zhao, Xinran Cao, Jinran Liu, Quan Han, Dijun Chen, Wen Lv, Yicheng Xie, Yang Sun

{"title":"Monkey multi-organ cell atlas exposed to estrogen.","authors":"Wen Fang, Jiao Qu, Wanjun Zhao, Xinran Cao, Jinran Liu, Quan Han, Dijun Chen, Wen Lv, Yicheng Xie, Yang Sun","doi":"10.1093/lifemedi/lnae012","DOIUrl":"10.1093/lifemedi/lnae012","url":null,"abstract":"Awareness of estrogen's effects on health is broadening rapidly. The effects of long-term high levels of estrogen on the body involve multiple organs. Here, we used both single-cell chromatin accessibility and RNA sequencing data to analyze the potential effect of estrogen on major organs. The integrated cell map enabled in-depth dissection and comparison of molecular dynamics, cell-type compositions, and cellular heterogeneity across multiple tissues and organs under estrogen stimulation. We also inferred pseudotime cell trajectories and cell-cell communications to uncover key molecular signatures underlying their cellular processes in major organs in response to estrogen. For example, estrogen could induce the differentiation of IFIT3 + neutrophils into S100A9 + neutrophils involved in the function of endosome-to-lysosome transport and the multivesicular body sorting pathway in liver tissues. Furthermore, through integration with human genome-wide association study data, we further identified a subset of risk genes during disease development that were induced by estrogen, such as AKT1 (related to endometrial cancer), CCND1 (related to breast cancer), HSPH1 (related to colorectal cancer), and COVID-19 and asthma-related risk genes. Our work uncovers the impact of estrogen on the major organs, constitutes a useful resource, and reveals the contribution and mechanism of estrogen to related diseases.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"3 2","pages":"lnae012"},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11749546/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143054563","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Tracing TMEM106B fibril deposition in aging and Parkinson’s disease with dementia brains 追踪衰老和帕金森病痴呆大脑中的 TMEM106B 纤维沉积情况

Life medicine Pub Date : 2024-03-07 DOI: 10.1093/lifemedi/lnae011

Wanbing Zhao, Yun Fan, Qinyue Zhao, Zhen Fan, Jue Zhao, Wenbo Yu, Wensheng Li, Dan Li, Cong Liu, Jian Wang

{"title":"Tracing TMEM106B fibril deposition in aging and Parkinson’s disease with dementia brains","authors":"Wanbing Zhao, Yun Fan, Qinyue Zhao, Zhen Fan, Jue Zhao, Wenbo Yu, Wensheng Li, Dan Li, Cong Liu, Jian Wang","doi":"10.1093/lifemedi/lnae011","DOIUrl":"https://doi.org/10.1093/lifemedi/lnae011","url":null,"abstract":"\u0000 Transmembrane protein 106B (TMEM106B), previously identified as a risk factor in frontotemporal lobar degeneration, has recently been detected to form fibrillar aggregates in the brains of patients with various neurodegenerative diseases (NDs) and normal elders. While, the specifics of when and where TMEM106B fibrils accumulate in human brains, as well as their connection to aging and disease progression, remain poorly understood. Here, we identified an antibody (NBP1-91311) that directly binds to TMEM106B fibrils extracted from the brain in vitro and to Thioflavin S positive TMEM106B fibrillar aggregates in brain sections. We discovered that TMEM106B fibrils deposit in the human brain in an age-dependent manner. Notably, the TMEM106B fibril load in the brains of Parkinson’s disease with dementia patients was significantly higher than in age-matched elders. Additionally, we found that TMEM106B fibrils predominantly accumulate in astrocytes and neurons and do not co-localize with the pathological deposition formed by other amyloid proteins such as α-synuclein, Aβ, and Tau. Our work provides a comprehensive analysis of the burden and cellular distribution of TMEM106B fibrils in human brains, underscoring the impact of both aging and disease conditions on TMEM106B fibril deposition. This highlights the potential significance of TMEM106B fibrils in various age-related NDs.","PeriodicalId":74073,"journal":{"name":"Life medicine","volume":"29 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140260556","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

Osteoporosis under psychological stress: mechanisms and therapeutics 心理压力下的骨质疏松症：机制与疗法

Life medicine Pub Date : 2024-03-07 DOI: 10.1093/lifemedi/lnae009

Hao-Kun Xu, Jie-Xi Liu, Ze-Kai Zhou, Chen-Xi Zheng, B. Sui, Yuan Yuan, Liang Kong, Yan Jin, Ji Chen

引用次数: 0

When synthetic biology meets medicine 当合成生物学遇上医学

Life medicine Pub Date : 2024-03-06 DOI: 10.1093/lifemedi/lnae010

Yuge Feng, Cong Su, Guobin Mao, Baoting Sun, Yizhi Cai, Junbiao Dai, Yingxin Ma

引用次数: 0