CCN3

更新于：2025-05-07

基本信息

别名

CCN family member 3、CCN3、cellular communication network factor 3

+ [9]

简介

Immediate-early protein playing a role in various cellular processes including proliferation, adhesion, migration, differentiation and survival (PubMed:12050162, PubMed:12695522, PubMed:15181016, PubMed:15611078, PubMed:21344378). Acts by binding to integrins or membrane receptors such as NOTCH1 (PubMed:12695522, PubMed:15611078, PubMed:21344378). Essential regulator of hematopoietic stem and progenitor cell function (PubMed:17463287). Inhibits myogenic differentiation through the activation of Notch-signaling pathway (PubMed:12050162). Inhibits vascular smooth muscle cells proliferation by increasing expression of cell-cycle regulators such as CDKN2B or CDKN1A independently of TGFB1 signaling (PubMed:20139355). Ligand of integrins ITGAV:ITGB3 and ITGA5:ITGB1, acts directly upon endothelial cells to stimulate pro-angiogenic activities and induces angiogenesis. In endothelial cells, supports cell adhesion, induces directed cell migration (chemotaxis) and promotes cell survival (PubMed:12695522). Also plays a role in cutaneous wound healing acting as integrin receptor ligand. Supports skin fibroblast adhesion through ITGA5:ITGB1 and ITGA6:ITGB1 and induces fibroblast chemotaxis through ITGAV:ITGB5. Seems to enhance bFGF-induced DNA synthesis in fibroblasts (PubMed:15611078). Involved in bone regeneration as a negative regulator (By similarity). Enhances the articular chondrocytic phenotype, whereas it repressed the one representing endochondral ossification (PubMed:21871891). Impairs pancreatic beta-cell function, inhibits beta-cell proliferation and insulin secretion (By similarity). Plays a role as negative regulator of endothelial pro-inflammatory activation reducing monocyte adhesion, its anti-inflammatory effects occur secondary to the inhibition of NF-kappaB signaling pathway (PubMed:21063504). Contributes to the control and coordination of inflammatory processes in atherosclerosis (By similarity). Attenuates inflammatory pain through regulation of IL1B- and TNF-induced MMP9, MMP2 and CCL2 expression. Inhibits MMP9 expression through ITGB1 engagement (PubMed:21871891). Brain osteoanabolic hormone (By similarity). Drives osteogenesis in osteochondral skeletal stem cells (PubMed:38987585). During lactation, maintains the maternal skeleton and viability of offspring (By similarity).

关联

100 项与 CCN3 相关的临床结果

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100 项与 CCN3 相关的转化医学

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0 项与 CCN3 相关的专利（医药）

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346

项与 CCN3 相关的文献（医药）

2025-05-01·Current Molecular Medicine

CCN3/NOV Serum Levels in Non-alcoholic Fatty Liver Disease (NAFLD) Patients in Comparison with the Healthy Group and its Correlation with TNF-α and IL-6

Article

作者: Alizadeh, Shaban ; Jadidi, Yasaman ; Farrokhi, Vida ; Moradi, Nariman ; Alasvand, Ghazal ; Afrisham, Reza ; Fadaei, Reza

Introduction:Adipokine irregularity leads to inflammation, endothelial dysfunction, insulin resistance (IR), and Non-Alcoholic Fatty Liver Disease (NAFLD). Previous studies linked NOV/CCN3 to obesity, IR, and inflammation, but no research has explored the connection between CCN3 serum levels and NAFLD.Methods:This case-control study assessed CCN3, IL-6, adiponectin, and TNF-α serum levels in 80 NAFLD patients and 80 controls using ELISA kits. Biochemical parameters were measured with commercial kits and an auto analyzer.Results:NAFLD patients exhibited significantly higher CCN3 (2399.85 ± 744.53 vs. 1712.84 ± 478.19 ng/ml), TNF-α, and IL-6 levels, and lower adiponectin levels compared to controls (P<0.0001). In the NAFLD group, CCN3 showed positive correlations with FBG, insulin, HOMA-IR, and TNF-α. Binary logistic regression analysis revealed increased NAFLD risk in the adjusted model (OR [95% CI] = 1.220 [1.315-1.131]). A CCN3 cut-off value of 1898.0050 pg/mL differentiated NAFLD patients from controls with 78.8% sensitivity and 73.2% specificity.Conclusion:It was found that elevated CCN3 serum levels directly correlate with NAFLD incidence and inflammation markers (IL-6 and TNF-α). CCN3 could serve as a potential biomarker for NAFLD, but further research is needed to validate this finding and assess its clinical utility.

2025-03-01·Advanced Healthcare Materials

A Highly Bioactive Organic–Inorganic Nanoparticle for Activating Wnt10b Mediated Osteogenesis by Specifically Anchor CCN3 Protein

Article

作者: Lei, Bo ; Zhang, Liuyang ; Huang, Haohui ; Zhao, Fujian ; Wang, Chunhui ; Xu, Shijing ; Yang, Yulian ; Qiu, Yonghao

AbstractThe rapid and efficient bone regeneration is still in unsatisfactory outcomes, demonstrating alternative strategy and molecular mechanism is necessary. Nanoscale biomaterials have shown some promising results in enhancing bone regeneration, however, the detailed interaction mechanism between nanomaterial and cells/tissue formation is not clear. Herein, a molecular‐based inorganic–organic nanomaterial poly(citrate‐siloxane) (PCS) is reported which can rapidly enhance osteogenic differentiation and bone formation through a special interaction with the cellular surface communication network factor 3 (CCN3), further activating the Wnt10b/β‐catenin signaling pathway. Further studies revealed that the CCN3 is a key bridge protein for transmitting the osteoinductive effects of nano PCS into the intracellular compartment and activating Wnt10b. Specifically, the molecular mechanism studies confirmed that the inorganic silicon hydroxyl and the organic ester group can bound to the Thrombospondin‐1 (TSP‐1) and von Willebrand factor type C repeat module (vWC) structural domains of CCN3 respectively. The special material‐protein interaction induced a conformational change of CCN3 and activated the function of the TSP‐1 structural domain, which is further associated with the binding and activation of Wnt10b signaling. This study reveals the first targets of nanobiomaterials to promote tissue regeneration through cellular interactions and provides new ideas for the development of materiobiology.

2025-03-01·Journal of Dentistry

CircFak promotes mechanical force-induced osteogenesis via FAK/AKT phosphorylation

Article

作者: Wu, Fan ; Xie, Shule ; Lu, Yingjuan ; Li, Jinsong ; Cheng, Huilin ; Liang, Defeng ; Shi, Juanyi ; Wen, Zhihui

OBJECTIVESOrthodontic treatment is widely applied for addressing orofacial skeletal deformities, with the remodeling of the alveolar bone under mechanical force being the key factor. FAK is essential for cellular response to mechanical force. However, the function of circFak has never been reported. In this study, the microarrays showed that circFak may affect osteogenesis under mechanical force. We aimed to verify the effect of circFak in force-related bone remodeling and investigate the underlying mechanisms.METHODSArraystar microarrays were used to identify differentially expressed circRNAs and microRNAs in response to mechanical stress. The subcellular distribution of circFak was analyzed via RT‒qPCR and FISH. ALP and ARS staining assays were performed to investigate the effects of circFak on osteogenesis. RNA sequencing, bioinformatics analysis, dual-luciferase reporter assays, and RNA immunoprecipitation were accomplished to discover the molecular mechanisms of circFak. AAV-sh-circFak mouse models with tooth movements were established. The role of circFak under mechanical force in vivo was assessed via immunofluorescence and micro-CT analyses.RESULTSCircFak expression was significantly upregulated under mechanical force. Osteogenic capacity of osteoblasts was positively correlated with the level of circFak. CircFak promoted mechanical force-induced osteogenesis through miR-425-5p/Ccn3 pathway, and further stimulated the phosphorylation of its parental sourced protein FAK. Our murine models showed that AAV-mediated circFak silencing suppressed osteogenesis.CONCLUSIONCircFak could obviously promote osteogenesis under mechanical force and may possess ability to become a novel biomarker for prognosis of orthodontic treatments.

项与 CCN3 相关的新闻（医药）

2024-07-31

·生物谷

哺乳期奇迹激素CCN3！Nature | 新发现的母体脑激素CCN3可增强哺乳动物的骨密度和骨强度

在一项新的研究中，来自加州大学旧金山分校和加州大学戴维斯分校的研究人员解决了一个长期存在的难题，即哺乳期女性如何在大量钙质转移到乳汁中滋养婴儿的同时，依然保持骨骼的健康与强度？这项研究揭示了一种此前未知的激素——“母体脑激素”（MBH），具体而言是一种名为CCN3的激素，它不仅能够增强哺乳期女性的骨骼，还可能促进骨折愈合，惠及更广泛的人群。相关研究结果于2024年7月10日在线发表在Nature期刊上，论文标题为“A maternal brain hormone that builds bone”。论文共同通讯作者、加州大学旧金山分校细胞分子药理学教授Holly Ingraham博士强调：“若非关注雌性小鼠，这一发现可能被完全忽略，这是生物医学研究领域常有的遗憾。这再次证明，全面探索雌雄两性全生命周期的生物学意义至关重要。” 全球逾2亿人深受骨质疏松症困扰，该病导致骨骼脆弱，易发骨折。尤其在女性绝经后，骨质疏松风险显著升高，归因于雌激素水平骤降，而雌激素对骨骼形成具有促进作用。尽管哺乳期雌激素水平同样低下，但骨质疏松及骨折却相对罕见，暗示另有关键因素促进骨骼生长。 Ingraham实验室先前研究揭示，特定雌性小鼠大脑区域中雌激素受体的阻断可显著增加骨量，而雄性小鼠未见此现象。他们曾推测，是某种血液因子在背后驱动骨骼异常增长，但当时却找不到这种关键因子。在这项新的研究中，Ingraham及其合作者对这种造骨激素进行了详尽的搜索，最终确定CCN3是导致突变雌性小鼠骨骼强壮的因素。最初，他们对这一结果感到惊讶，因为CCN3并不符合神经元分泌激素的典型特征。当他们在哺乳期雌性小鼠的同一脑区发现CCN3后，他们的疑虑消失了。如果这些特定神经元不分泌 CCN3，那么哺乳期雌性小鼠的骨质就会迅速流失，其幼仔的体重也会开始下降，这证实了这种激素在哺乳期维持骨骼健康的重要性。鉴于此，研究团队正式将CCN3命名为母体脑激素。通过进一步实验，研究人员发现，无论是年轻还是老龄的雌雄小鼠，通过提升体内CCN3水平，均能在数周内显著增强骨量与强度。即便在雌激素极度缺乏或年迈雌性小鼠中，CCN3亦能实现骨量翻倍以上的增长。图片来自Nature, 2024, doi:10.1038/s41586-024-07634-3 当Ingraham的科学合作者、加州大学戴维斯分校的Thomas Ambrosi博士对这些骨骼进行测试时，他对这些骨骼的强度感到惊讶。他解释说，“在某些情况下，过度矿化的骨骼未必更优；它们可能更为脆弱、更容易断裂。但当我们测试这些骨骼时，发现它们的骨骼比正常时要坚固得多。” 深入研究发现：CCN3能促进骨骼干细胞分化，加速新骨细胞生成。为检验CCN3对骨骼愈合的潜力，研究团队开发了一种水凝胶贴片，可直接贴敷于骨折处，在两周内促使体内缓慢释放CCN3。在老龄小鼠中，骨折愈合通常不佳，但含CCN3的水凝胶贴片显著促进了其骨折部位的新骨形成，加速愈合进程。Ambrosi表示：“我们从未见过如此卓越的矿化与愈合效果，未来有望将CCN3应用于软骨再生等领域。” 研究团队计划进一步探索CCN3的分子机制、母乳喂养女性的CCN3水平，及其在多种骨骼疾病治疗中的潜力。论文共同第一作者、加州大学旧金山分校内分泌科指导医师Muriel Babey博士热切期待CCN3在临床相关疾病中对骨代谢的影响。William Krause博士将与加州大学旧金山分校催化剂项目合作，推动研究成果转化。 Ingraham说，“骨质流失不仅发生在绝经后的妇女身上，而且经常发生在服用某些激素阻断剂的乳腺癌幸存者身上、或是年轻、训练有素的精英女运动员身上、以及髋部骨折后相对存活率比妇女低的老年男性身上。若CCN3均能在此类人群中提升骨量，将是一项激动人心的突破！” 参考资料： Muriel E. Babey et al. A maternal brain hormone that builds bone. Nature, 2024, doi:10.1038/s41586-024-07634-3. 本文仅用于学术分享，转载请注明出处。若有侵权，请联系微信：bioonSir 删除或修改！点击下方「阅读原文」，前往生物谷官网查询更多生物相关资讯~

2024-07-10

·drugs

Researchers Discover New Hormone That Builds Strong Bones

WEDNESDAY, July 10, 2024 -- A newly discovered hormone could help fight osteoporosis and quickly heal broken bones, researchers say. The research team identified Maternal Brain Hormone while trying to figure out why the bones of breastfeeding women remain relatively strong, even as calcium is stripped from the bones to support milk production. It turns out that the neurons of breastfeeding moms secrete Maternal Brain Hormone, and that this hormone protects their bone health. Bone mass and strength increased in both female and male mice when researchers boosted their levels of Maternal Brain Hormone, results show. Further, the hormone increased healing in bone fractures among elderly mice, essentially causing the broken bone to heal at a rate similar to that of a young mouse. “We’ve never been able to achieve this kind of mineralization and healing outcome with any other strategy,” researcher Thomas Ambrosi , an assistant professor at the University of California-Davis, said in a news release. “We’re really excited to follow it up and potentially apply (the hormone) in the context of other problems, such as regrowing cartilage.” Women are at high risk of osteoporosis during menopause because of declining levels of the female sex hormone estrogen, which normally promotes bone growth, researchers said in background notes. Estrogen levels are also low during breastfeeding, but those women are resistant to osteoporosis and broken bones, researchers said. This suggested that something other than estrogen promoted bone growth among them. Researchers eventually came across a hormone called CCN3 in a small brain region of lactating female mice. Without production of the hormone, these lactating mice rapidly lost bone and their babies began to lose weight – indicating that the hormone played a prominent role in maintain bone health. The research team gave CCN3 a new name, Maternal Brain Hormone. They found that in some female mice who were very old or without estrogen, the hormone was able to more than double bone mass. The findings were published July 10 in the journal Nature . Researchers plan to test the effectiveness of the hormone in treating a variety of bone conditions. “Bone loss happens not only in post-menopausal women but often occurs in breast cancer survivors that take certain hormone blockers; in younger, highly trained elite female athletes; and in older men whose relative survival rate is poorer than women after a hip fracture,” said senior researcher Holly Ingraham , a professor of cellular molecular pharmacology at the University of California, San Francisco (UCSF). “It would be incredibly exciting if CCN3 could increase bone mass in all these scenarios,” Ingraham concluded in a UCSF news release. Whatever your topic of interest, subscribe to our newsletters to get the best of Drugs.com in your inbox.

2024-04-18

·今日头条

聚焦特殊人群：母婴肠道菌群与健康

04月18日的《热心肠日报》，我们解读了 15 篇文献，关注：母婴，营养不良，产后抑郁，多组学，益生菌，膳食纤维，胞外囊泡，儿童便秘，质量，肠神经，结肠憩室，MRM Health，食品用菌种检验，来凯医药，越洋医药，雀巢。该篇日报由R·AI辅助创作生成，人工审核校对。母亲童年营养不良如何影响后代生长发育? Microbiome——[15.5] ① 营养不良导致的线性生长迟缓与不良健康结果相关，且童年经历生长迟缓的母亲更有可能生育生长迟缓的孩子，本研究探究了人类营养不良儿童的肠道菌群对后代生长和免疫功能的影响；② 使用健康或发育迟缓婴儿的菌群移植给无菌小鼠，这些小鼠的子代就继承了亲代的菌群，子代断奶后采用营养不良的饮食，构建出营养不良模型；③ 与健康生长轨迹儿童的肠道菌群相比，营养不良儿童的肠道菌群进行代际定植能导致小鼠后代生长迟缓、营养不良以及肠病免疫特征的发展，如肠绒毛变短、肝脏IGF-1水平降低以及小肠上皮内淋巴细胞和浆细胞的积聚；④ 在断奶后进行肠道菌群定植则对宿主表型影响较小；⑤ 研究结果支持了微生物在断奶阶段对免疫系统的影响对后期免疫功能至关重要的观点，并表明跨代肠道菌群定植是研究早期生命中肠道菌群依赖性生长和免疫变化的有效方法。【原文信息】 Colonization during a key developmental window reveals microbiota-dependent shifts in growth and immunity during undernutrition 2024-04-09 , doi: 10.1186/s40168-024-01783-3 浙大医学院：肠道菌群失调促进产后抑郁症新机制 Brain Behavior and Immunity——[15.1] ① 浙大医学院附属妇产科医院陈新忠团队揭示了肠道菌群失调通过海马体NLRP3介导的神经炎症促进产后抑郁症（PPD），并探究了肠-脑轴在抑郁行为中的潜在作用；② 利用卵巢切除的雌性小鼠构建激素停撤模型模拟人类PPD，发现激素停撤后小鼠出现类抑郁和焦虑行为，同时肠道菌群组成改变；③ 将PPD小鼠粪菌移植（FMT）给抗生素处理的小鼠，受体小鼠出现类抑郁和焦虑行为以及海马体的神经病理变化；④ 从健康小鼠到PPD小鼠的FMT减轻了类抑郁和焦虑行为，降低了NLRP3/caspase-1信号通路介导的炎症，增加了粪便短链脂肪酸（SCFAs）水平，改善了肠道菌群失调（增加产SCFA菌，减少Akk菌）；⑤ 海马体NLRP3的下调减轻了PPD小鼠的类抑郁行为，而海马齿状回NLRP3的过表达在健康小鼠中诱发了类抑郁行为，且来自健康小鼠的FMT未能减轻抑郁行为。【原文信息】 Gut microbiota dysbiosis contributes to depression-like behaviors via hippocampal NLRP3-mediated neuroinflammation in a postpartum depression mouse model 2024-04-08 , doi: 10.1016/j.bbi.2024.04.002 Nature子刊：婴儿及其母系谱系肠道菌群的多组学比较研究 Nature Communications——[16.6] ① 本研究通过多组学方法比较了婴儿肠道菌群及其母系谱系的特征，旨在探究肠道菌群在婴儿期的早期发展；② 利用两种独立的代谢组学平台和宏基因组学研究分析200名个体（包括0-12个月龄婴儿及其母亲和祖母）的粪便样本；③ 婴儿的肠道菌群在种群、功能和代谢组方面与成年人存在显著差异，婴儿的菌群多样性较低，且多种代谢物类别（如短链和支链脂肪酸）具有差异，这些差异与细菌种群的变化有关；④ 本研究为同一代际界限内肠道菌群的塑造提供了创新的生化见解，有助于改善儿童健康结果。【原文信息】 Comparative characterization of the infant gut microbiome and their maternal lineage by a multi-omics approach 2024-04-08 , doi: 10.1038/s41467-024-47182-y 孕期多菌株益生菌对宝宝肠道菌群发育有何影响？ Gut Microbes——[12.2] ① 开展了一项随机、双盲、安慰剂对照试验，探讨了50名孕期肥胖女性使用Vivomixx®多菌株益生菌对其婴儿肠道微生物组（GM）及围产期健康的影响；② 益生菌并未直接改变婴儿GM多样性或特定菌群的丰度，也未通过母婴垂直传递，但在益生菌组中观察到与肥胖相关的产气柯林斯菌属减少；③ 安慰剂组中与代谢健康相关的阿克曼菌属减少，提示母亲GM的间接群落效应可能影响婴儿；④ 出生后3天，婴儿GM受分娩方式和分娩期间使用的抗生素影响，顺产婴儿GM多样性增加，双歧杆菌属和拟杆菌属相对丰度升高，而剖宫产婴儿肠球菌属丰度降低。【原文信息】 Multi-strain probiotics during pregnancy in women with obesity influence infant gut microbiome development: results from a randomized, double-blind placebo-controlled study 2024-04-09 , doi: 10.1080/19490976.2024.2337968 孕期高纤维饮食或补充特定益生菌，可能有益于后代肠道健康 Gut Microbes——[12.2] ① 这项研究发现，孕期补充促进肠道内丁酸生成的调节因子（高纤维饮食或特定益生菌）能够保护后代成年后的结肠炎肠道损伤；② 给怀孕母鼠饲喂高纤维饮食，或者补充乳酸乳球菌乳脂亚种或鼠李糖乳杆菌GG，然后在它们后代成年后诱导慢性结肠炎；③ 孕期高纤维饮食或者补充乳酸乳球菌乳脂亚种，均可减轻结肠炎对后代造成的肠道损伤；④ 这些结果证实了孕期饮食干预可以影响后代的肠道健康，并将孕期饮食定义为增强后代肠道健康的治疗方法。【原文信息】 A high fiber diet or supplementation with Lactococcus lactis subspecies cremoris to pregnant mice confers protection against intestinal injury in adult offspring 2024-04-15 , doi: 10.1080/19490976.2024.2337317 母乳中的胞外囊泡可被新生儿肠道吸收 Journal of Extracellular Vesicles——[16] ① 开发出一套从人乳和新生儿肠道内容物中分离胞外囊泡（HMEVs）的方法，以验证HMEVs是否在新生儿消化过程中存活并被肠上皮细胞吸收；② HMEVs和消化液中的胞外囊泡（dEVs）具有典型的胞外囊泡形态，并富含CD81和CD9蛋白，但不含β-酪蛋白和乳清蛋白；③ HMEV和一些dEV片段含有乳腺来源蛋白BTN1A1，新生儿人类肠绒毛体通过网格蛋白依赖型内吞迅速摄取dEVs；④ 本研究结果表明，新生儿人类肠类器官能迅速吸收dEVs，部分通过胞饮作用进行。【原文信息】 Neonatal enteroids absorb extracellular vesicles from human milk-fed infant digestive fluid 2024-04-11 , doi: 10.1002/jev2.12422 Lancet子刊：12%的亚洲儿童患有便秘（荟萃分析） EClinicalMedicine——[15.1] ① 本系统综述和荟萃分析旨在评估亚洲儿童便秘的流行情况及其相关因素；② 纳入了50项研究，共计311,660名亚洲儿童数据，发现便秘的整体患病率为12.0%；③ 年龄是便秘发生的一个重要影响因素，青少年和1～9岁儿童的便秘患病率显著高于婴儿，但便秘患病率在性别和地理位置上无显著差异；④ 尽管纳入的研究使用了不同的诊断工具或定义导致结果的高度异质性，但本综述增加了关于亚洲儿童便秘的数据；⑤ 本研究揭示了亚洲儿童便秘的高患病率，为制定相关预防策略提供了依据。【原文信息】 Prevalence and determinants of constipation in children in Asia: a systematic review and meta-analysis 2024-04-08 , doi: 10.1016/j.eclinm.2024.102578 Nature子刊：从全球样本看人类肠道中质粒的分布与选择压力 Nature Communications——[16.6] ① 通过分析3467个人类肠道微生物组样本中的11086个质粒，揭示了质粒在人类肠道中的分布主要受到随机扩散的影响，但炎症性疾病会显著改变这一过程；② 仅有20-25%的质粒DNA在各种疾病状态下被选择性地保留，这限制了它们在宿主间的分布；③ 特定的质粒片段因其独特的生态功能而受到选择性压力的影响，这些片段在患有类似健康状况的个体群体中更常共享（如IBD患者）；④ 质粒片段包含重要基因，如铁运输机制，这是IBD的肠道特征标志，影响炎症的严重程度；⑤ 本研究结果强调了质粒作为携带影响细菌宿主和生态系统动态的重要基因库的载体，在人类肠道中的扩散和选择机制。【原文信息】 Plasmids in the human gut reveal neutral dispersal and recombination that is overpowered by inflammatory diseases 2024-04-11 , doi: 10.1038/s41467-024-47272-x Nature子刊：利用肠神经干细胞移植治疗结肠无神经节症的潜力如何？ Nature Communications——[16.6] ① 本研究评估了自体肠神经干细胞移植治疗小鼠结肠无神经节病的可行性和潜力；② 通过注射白喉毒素在小鼠中创造出结肠无神经节模型，从小肠分离出自体肠神经干细胞进行体外扩增和标记后，移植回无神经节的结肠段；③ 移植的肠神经干细胞在体内分化成神经元和胶质细胞，形成新的神经节，可恢复结肠收缩活动，并通过电场刺激和光遗传学得到证实；④ 该研究不仅证明了自体肠神经干细胞治疗结肠无神经节的可行性，也为临床应用这一再生细胞治疗方法奠定了基础。【原文信息】 Autologous cell transplantation for treatment of colorectal aganglionosis in mice 2024-03-20 , doi: 10.1038/s41467-024-46793-9 结肠憩室的基因组和转录组图谱分析 Gut——[24.5] ① 本研究通过基因组和转录组分析揭示了结肠憩室病的遗传和细胞决定因素，为理解其发病机制提供了新见解；② 对404名患有（N=172）和不患有（N=232）结肠憩室病患者的结肠组织进行DNA和RNA测序，发现38个基因表达差异和17个转录本使用变化与结肠憩室病相关，表明组织重塑是憩室形成的主要机制；③ 憩室形成主要与结肠中的基质和上皮细胞有关，包括内皮细胞、肌成纤维细胞、成纤维细胞、杯状细胞、绒毛细胞、肠细胞、神经元和胶质细胞；④ 孟德尔随机化分析发现CCN3、CRISPLD2、ENTPD7、PHGR1和TNFSF13五个基因可能对结肠憩室病有潜在的因果效应，其中憩室病例中证实ENTPD7表达上调；⑤ 结肠憩室病的严重程度与患有憩室炎的遗传倾向正相关。【原文信息】 Genetic and transcriptomic landscape of colonic diverticulosis 2024-03-04 , doi: 10.1136/gutjnl-2023-331267 MRM公布活菌药MH002治疗结肠袋炎2a期临床积极结果 ① 4月16日，MRM Health对外公布了活菌药MH002 2a期临床试验MH002-PC-201研究的顶线阳性结果；② MH002-PC-201研究旨在评估MH002治疗结肠袋炎患者安全性和耐受性问题；③ 研究结果显示，安全性无问题，同时患者临床缓解率达46%；④ MH002是一种由6株肠道共生菌组成的配方菌活菌药，能够修复肠壁屏障功能和重建肠道免疫稳态；⑤ 基于当前监管积极反馈结果，MRM Health公司计划启动MH002治疗溃疡性结肠炎2/3期临床试验。【原文信息】 MRM Health Reports Safety and Positive Efficacy Data in Pouchitis in Phase 2a Clinical Study with MH002 2024-04-17 , Businesswire 《食品用菌种检验鼠李糖乳酪杆菌检验 PMA-qPCR法》团标正式发布 ① 4月1日，由中国食品院牵头起草的《食品用菌种检验鼠李糖乳酪杆菌检验 PMA-qPCR法》团体标准正式发布并实施；② 该标准由中国食品科学技术学会组织起草，伊利、蒙牛和汤臣倍健等多家单位参与；③ 标准的建立是为了对食品用菌种进行精准鉴定和活菌定量，保障产品质量和生产过程一致性控制；④ PMA-qPCR法可准确、稳定、可靠地实现鼠李糖乳酪杆菌的精准鉴定和活菌计数。【原文信息】中国食品院牵头起草的T/CIFST 020-2024《食品用菌种检验鼠李糖乳酪杆菌检验 PMA-qPCR法》团体标准正式发布 2024-04-16 , 中国食品发酵工业研究院来凯医药宣布LAE102新药临床试验获FDA批准 ① 4月15日，来凯医药宣布其用于治疗肥胖症候选药物LAE102的新药临床试验（IND）获FDA批准；② LAE102是一种针对参与调控肌肉再生和脂代谢的新靶点ActRIIA的单克隆抗体；③ LAE102在临床前研究中已显示出增加肌肉减少脂肪的效果，且可与GLP-1受体激动剂联用；④ 2024年第一季度，来凯医药还向中国国家药品监督管理局药品审评中心（CDE）提交了LAE102用于治疗肥胖症的IND申请，并获得受理；⑤ 目前，来凯医药仍在开发其他候选药物，包括LAE103和LAE123，均针对肌肉再生及相关疾病。【原文信息】快讯 | 来凯LAE102肥胖适应症新药临床试验获FDA批准 2024-04-15 , 药智新闻越洋医药与Peptidery公司合作共同进军GLP-1市场 ① 4月8日，越洋医药与美国Peptidery公司在江苏泰州中国医药城签署产品战略合作协议；② 双方将结合各自技术和资源优势，共同推进GLP-1合作产品在全球的研发和商业化；③ Peptidery是一家专注于多肽药物创新、研发与生产的公司，致力于提供高质量、安全、有效的多肽产品；④ 越洋医药主营业务包括开发针对美国和中国市场的2类新药，帮助国内外客户提高NCE的成药性，为国内外客户开发缓控释新药及仿制药。【原文信息】越洋医药与美国药企签署战略合作协议共同进军GLP-1 2024-04-15 , 越洋医药雀巢青岛超高温灭菌奶项目奠基 ① 4月12日，雀巢青岛在莱西食品产业集聚区庆祝其成立30周年并奠基超高温灭菌奶项目；② 新增资扩产的高温灭菌奶项目总投资16亿元，计划分三期实施；③ 其中，一期预计于2025年6月投产，旨在提升奶制品生产能力；④ 该项目将满足国内增长的消费需求，进一步优化产业结构，并促进当地乳制品产业发展；⑤ 雀巢青岛自1994年成立以来，已建立液体乳和速溶咖啡生产基地及相关研发中心。【原文信息】雀巢青岛30周年庆暨超高温灭菌奶项目奠基 2024-04-15 , Foodaily 感谢本期日报的审核者：章台柳，RZN，圆圈儿，九卿臣，注册营养师陈彬林，Richard，lxx，Alex Zhang 点击阅读过去10天的日报： 0417 | 高分Nature子刊：汇集全球玩家力量，助力肠道微生物研究 0416 | 多文聚焦：保卫肠道，免疫细胞和菌群谁都不能少 0415 | Cell重磅综述：系统解析癌症复杂性，菌群作用不容小觑 0414 | 高分Cell子刊综述，一文讲透发酵食品 0413 | 3篇子刊重磅文章，解析微生物组治疗的现状与未来 0412 | 10文聚焦国内团队新成果，肠道和菌群研究多点开花 0411 | 今日Nature：抵御病菌感染，结肠细胞如何与T细胞协作？ 0410 | 今日Cell：首个大规模泛癌转移瘤菌群图谱重磅出炉 0409 | 高分Nature子刊：菌群产物药物研发取得新进展 0408 | 300万人数据："好"胆固醇与消化道癌症风险有何关联？

微生物疗法临床研究