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Biofilms and exopolysaccharides in Pseudomonas aeruginosa: pathogenesis, immune evasion, and lung-brain signaling during pneumonia. 铜绿假单胞菌的生物膜和外多糖:肺炎期间的致病机理、免疫逃避和肺脑信号传导。
IF 40.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-19 DOI: 10.1038/s41392-024-01902-4
Shuaibing Zhang, Pierre Stallforth
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引用次数: 0
Novel pathomechanistic insights into lysosomal storage disorders: how neuron-intrinsic cGAS-STING signaling drives disease progression. 溶酶体贮积症的新病理机制:神经元内在 cGAS-STING 信号是如何驱动疾病进展的?
IF 40.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-16 DOI: 10.1038/s41392-024-01901-5
Maximilian Frosch, Marco Prinz
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引用次数: 0
Robust neutralizing antibody response to the XBB.1.5 trivalent recombinant protein vaccine booster. XBB.1.5三价重组蛋白疫苗强化剂的强效中和抗体反应。
IF 40.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-16 DOI: 10.1038/s41392-024-01924-y
Bing-Dong Zhan, Xue-Dong Song, Xin Yu, Guo-Jian Yang, Sheng Wan, Mai-Juan Ma
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引用次数: 0
Branched-chain amino acid transaminase 1 confers EGFR-TKI resistance through epigenetic glycolytic activation. 支链氨基酸转氨酶1通过表观遗传的糖酵解激活赋予表皮生长因子受体-TKI耐药性。
IF 40.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-15 DOI: 10.1038/s41392-024-01928-8
Tao Zhang, Zilu Pan, Jing Gao, Qingqing Wu, Gang Bai, Yan Li, Linjiang Tong, Fang Feng, Mengzhen Lai, Yingqiang Liu, Peiran Song, Yi Ning, Haotian Tang, Wen Luo, Yi Chen, Yan Fang, Hui Zhang, Qiupei Liu, Yudi Zhang, Hua Wang, Zhiwei Chen, Yi Chen, Meiyu Geng, Hongbin Ji, Guilong Zhao, Hu Zhou, Jian Ding, Hua Xie

Third-generation EGFR tyrosine kinase inhibitors (TKIs), exemplified by osimertinib, have demonstrated promising clinical efficacy in the treatment of non-small cell lung cancer (NSCLC). Our previous work has identified ASK120067 as a novel third-generation EGFR TKI with remarkable antitumor effects that has undergone New Drug Application (NDA) submission in China. Despite substantial progress, acquired resistance to EGFR-TKIs remains a significant challenge, impeding the long-term effectiveness of therapeutic approaches. In this study, we conducted a comprehensive investigation utilizing high-throughput proteomics analysis on established TKI-resistant tumor models, and found a notable upregulation of branched-chain amino acid transaminase 1 (BCAT1) expression in both osimertinib- and ASK120067-resistant tumors compared with the parental TKI-sensitive NSCLC tumors. Genetic depletion or pharmacological inhibition of BCAT1 impaired the growth of resistant cells and partially re-sensitized tumor cells to EGFR TKIs. Mechanistically, upregulated BCAT1 in resistant cells reprogrammed branched-chain amino acid (BCAA) metabolism and promoted alpha ketoglutarate (α-KG)-dependent demethylation of lysine 27 on histone H3 (H3K27) and subsequent transcriptional derepression of glycolysis-related genes, thereby enhancing glycolysis and promoting tumor progression. Moreover, we identified WQQ-345 as a novel BCAT1 inhibitor exhibiting antitumor activity both in vitro and in vivo against TKI-resistant lung cancer with high BCAT1 expression. In summary, our study highlighted the crucial role of BCAT1 in mediating resistance to third-generation EGFR-TKIs through epigenetic activation of glycolysis in NSCLC, thereby supporting BCAT1 as a promising therapeutic target for the treatment of TKI-resistant NSCLC.

以奥希替尼为代表的第三代表皮生长因子受体酪氨酸激酶抑制剂(TKIs)在治疗非小细胞肺癌(NSCLC)方面取得了良好的临床疗效。我们之前的研究发现,ASK120067是一种新型的第三代表皮生长因子受体TKI,具有显著的抗肿瘤效果,目前已在中国提交新药申请(NDA)。尽管EGFR-TKIs取得了长足进展,但获得性耐药仍是一个重大挑战,阻碍了治疗方法的长期有效性。在这项研究中,我们利用高通量蛋白质组学分析对已建立的TKI耐药肿瘤模型进行了全面调查,发现与亲代TKI敏感的NSCLC肿瘤相比,奥希替尼和ASK120067耐药肿瘤中支链氨基酸转氨酶1(BCAT1)表达明显上调。对BCAT1进行基因耗竭或药物抑制可抑制耐药细胞的生长,并使肿瘤细胞对表皮生长因子受体TKIs部分再敏感。从机理上讲,耐药细胞中上调的BCAT1重编程了支链氨基酸(BCAA)代谢,促进了组蛋白H3(H3K27)上赖氨酸27(H3K27)的α-酮戊二酸(α-KG)依赖性去甲基化,随后抑制了糖酵解相关基因的转录,从而增强了糖酵解,促进了肿瘤进展。此外,我们发现WQQ-345是一种新型BCAT1抑制剂,对BCAT1高表达的TKI耐药肺癌具有体外和体内抗肿瘤活性。总之,我们的研究强调了 BCAT1 在 NSCLC 中通过糖酵解的表观遗传激活介导对第三代 EGFR-TKIs 耐药的关键作用,从而支持 BCAT1 成为治疗 TKI 耐药 NSCLC 的有前途的治疗靶点。
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引用次数: 0
Therapeutic advances of targeting receptor tyrosine kinases in cancer. 针对癌症受体酪氨酸激酶的治疗进展。
IF 40.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-14 DOI: 10.1038/s41392-024-01899-w
Ciprian Tomuleasa, Adrian-Bogdan Tigu, Raluca Munteanu, Cristian-Silviu Moldovan, David Kegyes, Anca Onaciu, Diana Gulei, Gabriel Ghiaur, Hermann Einsele, Carlo M Croce

Receptor tyrosine kinases (RTKs), a category of transmembrane receptors, have gained significant clinical attention in oncology due to their central role in cancer pathogenesis. Genetic alterations, including mutations, amplifications, and overexpression of certain RTKs, are critical in creating environments conducive to tumor development. Following their discovery, extensive research has revealed how RTK dysregulation contributes to oncogenesis, with many cancer subtypes showing dependency on aberrant RTK signaling for their proliferation, survival and progression. These findings paved the way for targeted therapies that aim to inhibit crucial biological pathways in cancer. As a result, RTKs have emerged as primary targets in anticancer therapeutic development. Over the past two decades, this has led to the synthesis and clinical validation of numerous small molecule tyrosine kinase inhibitors (TKIs), now effectively utilized in treating various cancer types. In this manuscript we aim to provide a comprehensive understanding of the RTKs in the context of cancer. We explored the various alterations and overexpression of specific receptors across different malignancies, with special attention dedicated to the examination of current RTK inhibitors, highlighting their role as potential targeted therapies. By integrating the latest research findings and clinical evidence, we seek to elucidate the pivotal role of RTKs in cancer biology and the therapeutic efficacy of RTK inhibition with promising treatment outcomes.

受体酪氨酸激酶(RTKs)是一类跨膜受体,由于其在癌症发病机制中的核心作用,已在肿瘤学临床上获得了极大的关注。基因改变,包括某些 RTKs 的突变、扩增和过表达,对创造有利于肿瘤发展的环境至关重要。发现 RTK 后,大量研究揭示了 RTK 失调是如何导致肿瘤发生的,许多癌症亚型的增殖、生存和发展都依赖于异常的 RTK 信号传导。这些发现为旨在抑制癌症关键生物通路的靶向疗法铺平了道路。因此,RTK 已成为抗癌疗法开发的主要靶点。在过去的二十年里,许多小分子酪氨酸激酶抑制剂(TKIs)被合成并通过临床验证,目前已被有效用于治疗各种癌症类型。在本手稿中,我们旨在全面了解癌症中的 RTKs。我们探讨了不同恶性肿瘤中特定受体的各种改变和过表达,并特别关注对当前 RTK 抑制剂的研究,强调它们作为潜在靶向疗法的作用。通过整合最新的研究成果和临床证据,我们试图阐明 RTK 在癌症生物学中的关键作用,以及 RTK 抑制剂的治疗效果。
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引用次数: 0
Drug tolerant persister cell plasticity in cancer: A revolutionary strategy for more effective anticancer therapies. 癌症中的耐药持久细胞可塑性:更有效抗癌疗法的革命性战略。
IF 40.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-14 DOI: 10.1038/s41392-024-01891-4
Jun He, Zejing Qiu, Jingjing Fan, Xiaohong Xie, Qinsong Sheng, Xinbing Sui

Non-genetic mechanisms have recently emerged as important drivers of anticancer drug resistance. Among these, the drug tolerant persister (DTP) cell phenotype is attracting more and more attention and giving a predominant non-genetic role in cancer therapy resistance. The DTP phenotype is characterized by a quiescent or slow-cell-cycle reversible state of the cancer cell subpopulation and inert specialization to stimuli, which tolerates anticancer drug exposure to some extent through the interaction of multiple underlying mechanisms and recovering growth and proliferation after drug withdrawal, ultimately leading to treatment resistance and cancer recurrence. Therefore, targeting DTP cells is anticipated to provide new treatment opportunities for cancer patients, although our current knowledge of these DTP cells in treatment resistance remains limited. In this review, we provide a comprehensive overview of the formation characteristics and underlying drug tolerant mechanisms of DTP cells, investigate the potential drugs for DTP (including preclinical drugs, novel use for old drugs, and natural products) based on different medicine models, and discuss the necessity and feasibility of anti-DTP therapy, related application forms, and future issues that will need to be addressed to advance this emerging field towards clinical applications. Nonetheless, understanding the novel functions of DTP cells may enable us to develop new more effective anticancer therapy and improve clinical outcomes for cancer patients.

非遗传机制近来已成为抗癌药物耐药性的重要驱动因素。其中,耐药持久细胞(DTP)表型正引起越来越多的关注,并在抗癌治疗中发挥着主要的非遗传作用。DTP 表型的特点是癌细胞亚群处于静止或慢细胞周期可逆状态,对刺激具有惰性特化,通过多种潜在机制的相互作用,在一定程度上耐受抗癌药物暴露,并在停药后恢复生长和增殖,最终导致耐药和癌症复发。因此,靶向 DTP 细胞有望为癌症患者提供新的治疗机会,尽管我们目前对这些 DTP 细胞在治疗耐药性方面的了解仍然有限。在这篇综述中,我们全面概述了 DTP 细胞的形成特点和潜在的耐药机制,基于不同的医学模型研究了 DTP 的潜在药物(包括临床前药物、旧药物的新用途和天然产物),并讨论了抗 DTP 治疗的必要性和可行性、相关应用形式以及未来推动这一新兴领域走向临床应用所需要解决的问题。尽管如此,了解 DTP 细胞的新功能或许能让我们开发出更有效的抗癌新疗法,改善癌症患者的临床治疗效果。
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引用次数: 0
Gefitinib (an EGFR tyrosine kinase inhibitor) plus anlotinib (an multikinase inhibitor) for untreated, EGFR-mutated, advanced non-small cell lung cancer (FL-ALTER): a multicenter phase III trial. 吉非替尼(表皮生长因子受体酪氨酸激酶抑制剂)加洛替尼(多激酶抑制剂)治疗未经治疗的表皮生长因子受体突变晚期非小细胞肺癌(FL-ALTER):一项多中心 III 期试验。
IF 40.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-13 DOI: 10.1038/s41392-024-01927-9
Hua-Qiang Zhou, Ya-Xiong Zhang, Gang Chen, Qi-Tao Yu, Hua Zhang, Guo-Wu Wu, Di Wu, Ying-Cheng Lin, Jun-Fei Zhu, Jian-Hua Chen, Xiao-Hua Hu, Bin Lan, Ze-Qiang Zhou, Hai-Feng Lin, Zi-Bing Wang, Xiao-Lin Lei, Suo-Ming Pan, Li-Ming Chen, Jian Zhang, Tian-Dong Kong, Ji-Cheng Yao, Xin Zheng, Feng Li, Li Zhang, Wen-Feng Fang

Dual inhibition of vascular endothelial growth factor and epidermal growth factor receptor (EGFR) signaling pathways offers the prospect of improving the effectiveness of EFGR-targeted therapy. In this phase 3 study (ClinicalTrial.gov: NCT04028778), 315 patients with treatment-naïve, EGFR-mutated, advanced non-small cell lung cancer (NSCLC) were randomized (1:1) to receive anlotinib or placebo plus gefitinib once daily on days 1-14 per a 3-week cycle. At the prespecified final analysis of progression-free survival (PFS), a significant improvement in PFS was observed for the anlotinib arm over the placebo arm (hazards ratio [HR] = 0.64, 95% CI, 0.48-0.80, P = 0.003). Particularly, patients with brain metastasis and those harboring EGFR amplification or high tumor mutation load gained significant more benefits in PFS from gefitinib plus anlotinib. The incidence of grade 3 or higher treatment-emergent adverse events was 49.7% of the patients receiving gefitinib plus anlotinib versus 31.0% of the patients receiving gefitinib plus placebo. Anlotinib plus gefitinib significantly improves PFS in patients with treatment-naïve, EGFR-mutated, advanced NSCLC, with a manageable safety profile.

对血管内皮生长因子和表皮生长因子受体(EGFR)信号通路的双重抑制有望提高EFGR靶向疗法的疗效。在这项3期研究(ClinicalTrial.gov: NCT04028778)中,315名未经治疗、表皮生长因子受体(EGFR)突变的晚期非小细胞肺癌(NSCLC)患者被随机(1:1)分配到接受安罗替尼或安慰剂加吉非替尼治疗,每天一次,每3周为一个周期,第1-14天为一个疗程。在预设的无进展生存期(PFS)最终分析中,观察到安洛替尼组的PFS显著优于安慰剂组(危险比[HR] = 0.64,95% CI,0.48-0.80,P = 0.003)。尤其是脑转移患者和表皮生长因子受体扩增或肿瘤突变负荷较高的患者,吉非替尼加安罗替尼治疗的PFS获益更大。接受吉非替尼加安洛替尼治疗的患者中,3级或3级以上治疗突发不良事件的发生率为49.7%,而接受吉非替尼加安慰剂治疗的患者中,3级或3级以上治疗突发不良事件的发生率为31.0%。安罗替尼联合吉非替尼能显著改善治疗无效、表皮生长因子受体突变的晚期NSCLC患者的PFS,且安全性可控。
{"title":"Gefitinib (an EGFR tyrosine kinase inhibitor) plus anlotinib (an multikinase inhibitor) for untreated, EGFR-mutated, advanced non-small cell lung cancer (FL-ALTER): a multicenter phase III trial.","authors":"Hua-Qiang Zhou, Ya-Xiong Zhang, Gang Chen, Qi-Tao Yu, Hua Zhang, Guo-Wu Wu, Di Wu, Ying-Cheng Lin, Jun-Fei Zhu, Jian-Hua Chen, Xiao-Hua Hu, Bin Lan, Ze-Qiang Zhou, Hai-Feng Lin, Zi-Bing Wang, Xiao-Lin Lei, Suo-Ming Pan, Li-Ming Chen, Jian Zhang, Tian-Dong Kong, Ji-Cheng Yao, Xin Zheng, Feng Li, Li Zhang, Wen-Feng Fang","doi":"10.1038/s41392-024-01927-9","DOIUrl":"10.1038/s41392-024-01927-9","url":null,"abstract":"<p><p>Dual inhibition of vascular endothelial growth factor and epidermal growth factor receptor (EGFR) signaling pathways offers the prospect of improving the effectiveness of EFGR-targeted therapy. In this phase 3 study (ClinicalTrial.gov: NCT04028778), 315 patients with treatment-naïve, EGFR-mutated, advanced non-small cell lung cancer (NSCLC) were randomized (1:1) to receive anlotinib or placebo plus gefitinib once daily on days 1-14 per a 3-week cycle. At the prespecified final analysis of progression-free survival (PFS), a significant improvement in PFS was observed for the anlotinib arm over the placebo arm (hazards ratio [HR] = 0.64, 95% CI, 0.48-0.80, P = 0.003). Particularly, patients with brain metastasis and those harboring EGFR amplification or high tumor mutation load gained significant more benefits in PFS from gefitinib plus anlotinib. The incidence of grade 3 or higher treatment-emergent adverse events was 49.7% of the patients receiving gefitinib plus anlotinib versus 31.0% of the patients receiving gefitinib plus placebo. Anlotinib plus gefitinib significantly improves PFS in patients with treatment-naïve, EGFR-mutated, advanced NSCLC, with a manageable safety profile.</p>","PeriodicalId":21766,"journal":{"name":"Signal Transduction and Targeted Therapy","volume":"9 1","pages":"215"},"PeriodicalIF":40.8,"publicationDate":"2024-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11319491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141971805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Current advance of nanotechnology in diagnosis and treatment for malignant tumors. 纳米技术在诊断和治疗恶性肿瘤方面的最新进展。
IF 40.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-12 DOI: 10.1038/s41392-024-01889-y
Bilan Wang, Shiqi Hu, Yan Teng, Junli Chen, Haoyuan Wang, Yezhen Xu, Kaiyu Wang, Jianguo Xu, Yongzhong Cheng, Xiang Gao

Cancer remains a significant risk to human health. Nanomedicine is a new multidisciplinary field that is garnering a lot of interest and investigation. Nanomedicine shows great potential for cancer diagnosis and treatment. Specifically engineered nanoparticles can be employed as contrast agents in cancer diagnostics to enable high sensitivity and high-resolution tumor detection by imaging examinations. Novel approaches for tumor labeling and detection are also made possible by the use of nanoprobes and nanobiosensors. The achievement of targeted medication delivery in cancer therapy can be accomplished through the rational design and manufacture of nanodrug carriers. Nanoparticles have the capability to effectively transport medications or gene fragments to tumor tissues via passive or active targeting processes, thus enhancing treatment outcomes while minimizing harm to healthy tissues. Simultaneously, nanoparticles can be employed in the context of radiation sensitization and photothermal therapy to enhance the therapeutic efficacy of malignant tumors. This review presents a literature overview and summary of how nanotechnology is used in the diagnosis and treatment of malignant tumors. According to oncological diseases originating from different systems of the body and combining the pathophysiological features of cancers at different sites, we review the most recent developments in nanotechnology applications. Finally, we briefly discuss the prospects and challenges of nanotechnology in cancer.

癌症仍然是人类健康的重大威胁。纳米医学是一个新兴的多学科领域,正在引起人们的广泛兴趣和研究。纳米医学在癌症诊断和治疗方面显示出巨大的潜力。专门设计的纳米粒子可用作癌症诊断中的造影剂,通过成像检查实现高灵敏度和高分辨率的肿瘤检测。纳米探针和纳米生物传感器的使用也使肿瘤标记和检测的新方法成为可能。通过合理设计和制造纳米药物载体,可以在癌症治疗中实现靶向给药。纳米颗粒能够通过被动或主动的靶向过程将药物或基因片段有效地输送到肿瘤组织,从而提高治疗效果,同时最大限度地减少对健康组织的伤害。同时,纳米颗粒还可用于放射增敏和光热疗法,以提高对恶性肿瘤的疗效。本综述对纳米技术如何用于诊断和治疗恶性肿瘤进行了文献综述和总结。根据源自人体不同系统的肿瘤疾病,并结合不同部位癌症的病理生理特点,我们回顾了纳米技术应用的最新进展。最后,我们简要讨论了纳米技术在癌症中的应用前景和挑战。
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引用次数: 0
Potassium voltage-gated channel subfamily H member 2 (KCNH2) is a promising target for incretin secretagogue therapies. 电压门控钾通道 H 亚家族成员 2(KCNH2)是一种很有前景的增量素分泌治疗靶点。
IF 40.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-12 DOI: 10.1038/s41392-024-01923-z
Ying-Chao Yuan, Hao Wang, Ze-Ju Jiang, Chang Liu, Qi Li, Si-Rui Zhou, Jin-Kui Yang

Derived from enteroendocrine cells (EECs), glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) are pivotal incretin hormones crucial for blood glucose regulation. Medications of GLP-1 analogs and GLP-1 receptor activators are extensively used in the treatment of type 2 diabetes (T2D) and obesity. However, there are currently no agents to stimulate endogenous incretin secretion. Here, we find the pivotal role of KCNH2 potassium channels in the regulation of incretin secretion. Co-localization of KCNH2 with incretin-secreting EECs in the intestinal epithelium of rodents highlights its significance. Gut epithelial cell-specific KCNH2 knockout in mice improves glucose tolerance and increases oral glucose-triggered GLP-1 and GIP secretion, particularly GIP. Furthermore, KCNH2-deficient primary intestinal epithelial cells exhibit heightened incretin, especially GIP secretion upon nutrient stimulation. Mechanistically, KCNH2 knockdown in EECs leads to reduced K+ currents, prolonged action potential duration, and elevated intracellular calcium levels. Finally, we found that dofetilide, a KCNH2-specific inhibitor, could promote incretin secretion in enteroendocrine STC-1 cells in vitro and in hyperglycemic mice in vivo. These findings elucidate, for the first time, the mechanism and application of KCNH2 in regulating incretin secretion by EECs. Given the therapeutic promise of GLP-1 and GIP in diabetes and obesity management, this study advances our understanding of incretin regulation, paving the way for potential incretin secretagogue therapies in the treatment of diabetes and obesity.

胰高血糖素样肽-1(GLP-1)和葡萄糖依赖性胰岛素促肽(GIP)来源于肠内分泌细胞(EECs),是对血糖调节至关重要的增量激素。GLP-1 类似物和 GLP-1 受体激活剂被广泛用于治疗 2 型糖尿病(T2D)和肥胖症。然而,目前还没有刺激内源性增量素分泌的药物。在这里,我们发现了 KCNH2 钾通道在增量素分泌调节中的关键作用。KCNH2 与啮齿动物肠上皮细胞中分泌增量素的 EECs 共定位,凸显了其重要性。小鼠肠上皮细胞特异性 KCNH2 基因敲除可改善葡萄糖耐量,增加口服葡萄糖触发的 GLP-1 和 GIP 分泌,尤其是 GIP。此外,缺失 KCNH2 的原代肠上皮细胞在营养素刺激下表现出增量素分泌增加,尤其是 GIP 分泌增加。从机理上讲,KCNH2 在肠上皮细胞中的敲除会导致 K+ 电流减少、动作电位持续时间延长和细胞内钙水平升高。最后,我们发现多非利特(一种 KCNH2 特异性抑制剂)能促进肠内分泌 STC-1 细胞体外和高血糖小鼠体内的增量素分泌。这些发现首次阐明了 KCNH2 在调节肠内分泌细胞分泌增量素中的机制和应用。鉴于 GLP-1 和 GIP 在糖尿病和肥胖症治疗中的治疗前景,这项研究增进了我们对增量素调节的了解,为治疗糖尿病和肥胖症的潜在增量素促泌剂疗法铺平了道路。
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引用次数: 0
Nascent mRNA damage: depot and disposal. 新的 mRNA 损伤:仓库和处置。
IF 40.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-08-09 DOI: 10.1038/s41392-024-01900-6
Mark Helm, Marie-Luise Winz
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引用次数: 0
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Signal Transduction and Targeted Therapy
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