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Ubiquitination in pyroptosis pathway: A potential therapeutic target for sepsis 热蛋白沉积途径中的泛素化:败血症的潜在治疗靶点
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.cytogfr.2024.09.001
Yan Liao , Wangzheqi Zhang , Miao Zhou , Chenglong Zhu , Zui Zou
Sepsis remains a significant clinical challenge, causing numerous deaths annually and representing a major global health burden. Pyroptosis, a unique form of programmed cell death characterized by cell lysis and the release of inflammatory mediators, is a crucial factor in the pathogenesis and progression of sepsis, septic shock, and organ dysfunction. Ubiquitination, a key post-translational modification influencing protein fate, has emerged as a promising target for managing various inflammatory conditions, including sepsis. This review integrates the current knowledge on sepsis, pyroptosis, and the ubiquitin system, focusing on the molecular mechanisms of ubiquitination within pyroptotic pathways activated during sepsis. By exploring how modulating ubiquitination can regulate pyroptosis and its associated inflammatory signaling pathways, this review provides insights into potential therapeutic strategies for sepsis, highlighting the need for further research into these complex molecular networks.
败血症仍然是一项重大的临床挑战,每年造成无数人死亡,是全球健康的主要负担。脓毒症是一种独特的程序性细胞死亡,其特点是细胞裂解和释放炎症介质,是脓毒症、脓毒性休克和器官功能障碍发病和进展的关键因素。泛素化是影响蛋白质命运的一种关键的翻译后修饰,已成为治疗包括败血症在内的各种炎症的一个有前途的靶点。本综述整合了目前有关脓毒症、热毒血症和泛素系统的知识,重点关注脓毒症期间激活的热毒血症通路中泛素化的分子机制。本综述通过探讨泛素化调节如何调控热蛋白沉积及其相关的炎症信号通路,为脓毒症的潜在治疗策略提供了见解,并强调了进一步研究这些复杂分子网络的必要性。
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引用次数: 0
Adeno-associated virus therapies: Pioneering solutions for human genetic diseases 腺相关病毒疗法:人类遗传疾病的开创性解决方案。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.cytogfr.2024.09.003
Dequan Liu , Tian Li , Lei Liu , Xiangyu Che , Xiaorui Li , Chang Liu , Guangzhen Wu
Adeno-associated virus (AAV) has emerged as a fundamental component in the gene therapy landscape, widely acknowledged for its effectiveness in therapeutic gene delivery. The success of AAV-based therapies, such as Luxturna and Zolgensma, underscores their potential as a leading vector in gene therapy. This article provides an in-depth review of the development and mechanisms of AAV vector-based therapies, offering a comprehensive analysis of the latest clinical trial outcomes in central nervous system (CNS) diseases, ocular conditions, and hemophilia, where AAV therapies have shown promising results. Additionally, we discusse the selection of administration methods and serotypes tailored to specific diseases. Our objective is to showcase the innovative applications and future potential of AAV-based gene therapy, laying the groundwork for continued clinical advancements.
腺相关病毒(AAV)已成为基因治疗领域的基本组成部分,其在治疗基因递送方面的有效性已得到广泛认可。以 AAV 为基础的疗法(如 Luxturna 和 Zolgensma)取得的成功凸显了其作为基因疗法主要载体的潜力。本文深入评述了基于 AAV 载体的疗法的发展和机制,全面分析了 AAV 疗法在中枢神经系统(CNS)疾病、眼部疾病和血友病方面的最新临床试验结果,这些领域的 AAV 疗法都取得了可喜的成果。此外,我们还讨论了针对特定疾病的给药方法和血清型的选择。我们的目标是展示基于 AAV 的基因疗法的创新应用和未来潜力,为继续推进临床研究奠定基础。
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引用次数: 0
Molecular mechanisms of regulation of IL-1 and its receptors 调节 IL-1 及其受体的分子机制。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.cytogfr.2024.09.004
J.V. Zhukova , J.A. Lopatnikova , A.A. Alshevskaya , S.V. Sennikov
Interleukin 1 (IL-1) is a pro-inflammatory cytokine that plays a key role in the development and regulation of nonspecific defense and specific immunity. However, its regulatory influence extends beyond inflammation and impacts a range of immune and non-immune processes. The involvement of IL-1 in numerous biological processes, including modulation of inflammation, necessitates strict regulation at multiple levels. This review focuses on these regulatory processes and discusses their underlying mechanisms. IL-1 activity is controlled at various levels, including receptor binding, gene transcription, expression as inactive proforms, and regulated post-translational processing and secretion. Regulation at the level of the receptor expression - alternative splicing, tissue-specific isoforms, and gene polymorphism - is also crucial to IL-1 functional activity. Understanding these regulatory features of IL-1 will not only continue to shape future research directions but will also highlight promising therapeutic strategies to modulate the biological effects of IL-1.
白细胞介素 1(IL-1)是一种促炎细胞因子,在非特异性防御和特异性免疫的发展和调节中发挥着关键作用。然而,它的调节作用超出了炎症范围,对一系列免疫和非免疫过程都有影响。IL-1 参与了许多生物过程,包括炎症的调节,因此有必要在多个层面进行严格的调控。本综述将重点讨论这些调控过程及其内在机制。IL-1 的活性在不同水平上受到控制,包括受体结合、基因转录、以非活性原形表达以及翻译后处理和分泌调节。受体表达水平的调控--替代剪接、组织特异性异构体和基因多态性--对 IL-1 的功能活性也至关重要。了解 IL-1 的这些调控特征不仅将继续塑造未来的研究方向,还将凸显调节 IL-1 生物效应的有前途的治疗策略。
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引用次数: 0
Mechanisms of Rho GTPases in regulating tumor proliferation, migration and invasion Rho GTPases 调节肿瘤增殖、迁移和侵袭的机制。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.cytogfr.2024.09.002
Cheng Liu , Shutao Chen , Yu Zhang , Xinyi Zhou , Haiwei Wang , Qigui Wang , Xi Lan
The occurrence of most cancers is due to the clonal proliferation of tumor cells, immune evasion, and the ability to spread to other body parts. Rho GTPases, a family of small GTPases, are key regulators of cytoskeleton reorganization and cell polarity. Additionally, Rho GTPases are key proteins that induce the proliferation and metastasis of tumor cells. This review focuses on the complex regulatory mechanisms of Rho GTPases, exploring their critical role in promoting tumor cell proliferation and dissemination. Regarding tumor cell proliferation, attention is given to the role of Rho GTPases in regulating the cell cycle and mitosis. In terms of tumor cell dissemination, the focus is on the role of Rho GTPases in regulating cell migration and invasion. Overall, this review elucidates the mechanisms of Rho GTPases members in the development of tumor cells, aiming to provide theoretical references for the treatment of mammalian tumor diseases and related applications.
大多数癌症的发生都是由于肿瘤细胞的克隆增殖、免疫逃避以及向身体其他部位扩散的能力。Rho GTPases 是一种小型 GTPases,是细胞骨架重组和细胞极性的关键调节因子。此外,Rho GTPases 还是诱导肿瘤细胞增殖和转移的关键蛋白。本综述将重点关注 Rho GTPases 的复杂调控机制,探讨它们在促进肿瘤细胞增殖和扩散方面的关键作用。在肿瘤细胞增殖方面,重点关注 Rho GTPases 在调节细胞周期和有丝分裂中的作用。在肿瘤细胞扩散方面,重点关注 Rho GTPases 在调节细胞迁移和侵袭方面的作用。总之,这篇综述阐明了 Rho GTPases 成员在肿瘤细胞发展过程中的作用机制,旨在为哺乳动物肿瘤疾病的治疗及相关应用提供理论参考。
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引用次数: 0
Glioblastoma-associated macrophages: A key target in overcoming glioblastoma therapeutic resistance 胶质母细胞瘤相关巨噬细胞:克服胶质母细胞瘤耐药性的关键靶点
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.cytogfr.2024.10.009
Aymane Kricha, Najat Bouchmaa, Sanae Ben Mkaddem, Abdellatif Abbaoui, Reda Ben Mrid, Rachid El Fatimy
Glioblastoma multiforme (GBM) is recognized as the most aggressive and malignant form of brain cancer, characterized by a highly heterogeneous phenotype, poor prognosis, and a median survival time of less than 16 months. Recent studies have highlighted the critical role of glioblastoma-associated macrophages (GAMs) in promoting tumor progression and resistance not only to immunotherapy but also to radiotherapy and chemotherapy. GAMs actively suppress immune responses, promote angiogenesis, facilitate tumor metastasis, and induce therapy resistance, through various mechanisms such as cytokines production, signaling pathways regulation, and angiogenesis. In this context, understanding these regulatory mechanisms is essential for developing efficient therapies. Preclinical studies have investigated diverse approaches to target these cells, both as monotherapies or in combination with other treatments. While these approaches have shown promise in strengthening antitumor immune responses in animal models, their clinical success remains to be fully determined. Herein, we provide a comprehensive overview of GAMs's role in GBM therapeutic resistance and summarizes existing approaches to target GAMs in overcoming tumor resistance.
多形性胶质母细胞瘤(GBM)被认为是最具侵袭性的恶性脑癌,其特点是表型高度异质性、预后差、中位生存期不到 16 个月。最近的研究突显了胶质母细胞瘤相关巨噬细胞(GAMs)在促进肿瘤进展和抵抗免疫疗法以及放疗和化疗方面的关键作用。GAMs 通过产生细胞因子、调节信号通路和血管生成等多种机制,积极抑制免疫反应、促进血管生成、促进肿瘤转移和诱导耐药性。在这种情况下,了解这些调控机制对于开发高效疗法至关重要。临床前研究已经研究了针对这些细胞的多种方法,既可作为单一疗法,也可与其他疗法联合使用。虽然这些方法已在动物模型中显示出加强抗肿瘤免疫反应的前景,但其临床成功与否仍有待全面确定。在此,我们全面概述了 GAMs 在 GBM 治疗耐药性中的作用,并总结了针对 GAMs 克服肿瘤耐药性的现有方法。
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引用次数: 0
Distinct roles of MIF in the pathogenesis of ischemic heart disease MIF 在缺血性心脏病发病机制中的不同作用。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.cytogfr.2024.10.005
Ling Zhao , Bang-Hao Zhao , Amanguli Ruze , Qiu-Lin Li , An-Xia Deng , Xiao-Ming Gao
The role of macrophage migration inhibitory factor (MIF) as a multifunctional cytokine in immunomodulation and inflammatory response is increasingly appreciated. Ischemic heart disease (IHD), the leading cause of global mortality, remains a focal point of research owing to its intricate pathophysiology. MIF has been identified as a critical player in IHD, where it exerts distinct roles. On one hand, MIF plays a protective role by enhancing energy metabolism through activation of AMPK, resisting oxidative stress, inhibiting activation of the JNK pathway, and maintaining intracellular calcium ion homeostasis. Additionally, MIF exerts protective effects through mesenchymal stem cells and exosomes. On the other hand, MIF can assume a pro-inflammatory role, which contributes to the exacerbation of IHD's development and progression. Furthermore, MIF levels significantly increase in IHD patients, and its genetic polymorphisms are positively correlated with prevalence and severity. These findings position MIF as a potential biomarker and therapeutic target in the management of IHD. This review summarizes the structure, source, signaling pathways and biological functions of MIF and focuses on its roles and clinical characteristics in IHD. The genetic variants of MIF associated with IHD is also discussed, providing more understandings of its complex interplay in the disease's pathology.
巨噬细胞迁移抑制因子(MIF)是一种多功能细胞因子,在免疫调节和炎症反应中的作用日益受到重视。缺血性心脏病(IHD)是导致全球死亡的主要原因,由于其病理生理学错综复杂,它仍然是研究的焦点。MIF 被认为是缺血性心脏病的关键因素,在其中发挥着不同的作用。一方面,MIF 通过激活 AMPK 加强能量代谢、抵抗氧化应激、抑制 JNK 通路的激活以及维持细胞内钙离子的平衡,从而发挥保护作用。此外,MIF 还通过间充质干细胞和外泌体发挥保护作用。另一方面,MIF 可发挥促炎作用,从而加剧 IHD 的发展和恶化。此外,IHD 患者体内的 MIF 水平明显升高,其基因多态性与发病率和严重程度呈正相关。这些发现使 MIF 成为治疗 IHD 的潜在生物标志物和治疗靶点。本综述总结了 MIF 的结构、来源、信号传导途径和生物功能,并重点讨论了其在 IHD 中的作用和临床特征。此外,还讨论了与 IHD 相关的 MIF 基因变异,使人们对其在疾病病理中的复杂相互作用有了更多的了解。
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引用次数: 0
The role of transforming growth factor β in cervical carcinogenesis 转化生长因子β在宫颈癌变中的作用。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.cytogfr.2024.10.006
Kleber Paiva Trugilo , Guilherme Cesar Martelossi Cebinelli , Eliza Pizarro Castilha , Mariane Ricciardi da Silva , Fernanda Costa Brandão Berti , Karen Brajão de Oliveira
Human papillomavirus (HPV) is involved in virtually all cases of cervical cancer. However, HPV alone is not sufficient to cause malignant development. The effects of chronic inflammation and the interaction of immune components with the microenvironment infected with the high-risk HPV type (HR) may contribute to cancer development. Transforming growth factor β (TGFB) appears to play an important role in cervical carcinogenesis. Protein and mRNA levels of this cytokine gradually increase as normal tissue develops into malignant tissue and are closely related to the severity of HPV infection. At the onset of infection, TGFB can inhibit the proliferation of infected cells and viral amplification by inhibiting cell growth and downregulating the transcriptional activity of the long control region (LCR) of HPV, thereby reducing the expression of early genes. When infected cells progress to a malignant phenotype, the response to the cell growth inhibitory effect of TGFB1 is lost and the suppression of E6 and E7 expression decreases. Subsequently, TGFB1 expression is upregulated by high levels of E6 and E7 oncoproteins, leading to an increase in TGFB1 in the tumor microenvironment, where this molecule promotes epithelial-to-mesenchymal transition (EMT), cell motility, angiogenesis, and immunosuppression. This interaction between HPV oncoproteins and TGFB1 is an important mechanism promoting the development and progression of cervical cancer.
几乎所有宫颈癌病例都与人类乳头瘤病毒(HPV)有关。然而,仅靠 HPV 并不足以导致恶性发展。慢性炎症的影响以及免疫成分与感染高危型 HPV(HR)的微环境的相互作用可能会导致癌症的发生。转化生长因子β(TGFB)似乎在宫颈癌的发生中起着重要作用。当正常组织发展为恶性组织时,这种细胞因子的蛋白和 mRNA 水平会逐渐升高,并且与 HPV 感染的严重程度密切相关。在感染初期,TGFB 可通过抑制细胞生长和下调 HPV 长控制区(LCR)的转录活性,从而降低早期基因的表达,抑制感染细胞的增殖和病毒的扩增。当受感染的细胞发展到恶性表型时,TGFB1 对细胞生长抑制作用的反应就会消失,对 E6 和 E7 表达的抑制作用也会减弱。随后,高水平的 E6 和 E7 肿瘤蛋白会上调 TGFB1 的表达,导致肿瘤微环境中的 TGFB1 增加,而这种分子会促进上皮细胞向间质转化(EMT)、细胞运动、血管生成和免疫抑制。HPV 癌蛋白与 TGFB1 之间的这种相互作用是促进宫颈癌发生和发展的重要机制。
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引用次数: 0
I don’t know about you, but I’m feeling IL-22 我不知道你怎么想,但我感觉到了 IL-22。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.cytogfr.2024.11.001
Logan S. Dean , Alissa N. Threatt , Kaylee Jones , Emmanuel O. Oyewole , Morgan Pauly , Maëlis Wahl , Melea Barahona , Rose W. Reiter , Tara M. Nordgren
Defense of the human body against damaging and pathogenic insults is a heavily regulated affair. A primary mechanism of defense at sites of insult are soluble mediators whose defensive maneuvers increase barrier integrity and promote pro-reparative and resolution processes. IL-22 is a cytokine in the IL-10 cytokine family that has garnered increased attention in recent years due to its intimate link in promoting resolution of inflammatory insults, while simultaneously being over expressed in certain fibrotic and chronic inflammatory-skewed diseases. The spatial action of IL-22 centers around the barrier sites of the body, including the skin, lungs, and gut mucosa. As such, a detailed understanding of the role of this cytokine, the producers and responders, and the diseases resulting from over- or under-expression have prominent impacts on a variety of disease outcomes. Herein we present a comprehensive review of IL-22; from historical perspectives and initial discovery, as well as more recent data that dramatically expands on the cellular sources and impact of this cytokine. We aim to showcase the duality of IL-22 and highlight addressable gaps in the field of IL-22 crosstalk and impacts at the ever-important mucosal and tissue barrier sites.
人体对破坏性和致病性损伤的防御是一个受到严格调控的过程。受损部位的主要防御机制是可溶性介质,其防御作用可提高屏障的完整性,促进恢复和修复过程。IL-22是IL-10细胞因子家族中的一种细胞因子,由于其与促进炎症损伤的恢复密切相关,同时在某些纤维化和慢性炎症倾斜性疾病中过度表达,因此近年来受到越来越多的关注。IL-22 的作用空间集中在人体的屏障部位,包括皮肤、肺部和肠道粘膜。因此,详细了解这种细胞因子的作用、产生者和响应者,以及因表达过高或过低而导致的疾病,对各种疾病的结果都有显著影响。在此,我们对 IL-22 进行了全面的回顾;从历史角度和最初的发现,以及最近的数据,这些数据极大地扩展了这种细胞因子的细胞来源和影响。我们的目的是展示 IL-22 的双重性,并强调 IL-22 在粘膜和组织屏障部位的串扰和影响领域存在的空白。
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引用次数: 0
Impact of chronic stress on intestinal mucosal immunity in colorectal cancer progression 慢性压力对结直肠癌进展过程中肠粘膜免疫的影响
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.cytogfr.2024.10.007
Shengya Yang , Ying Li , Yingru Zhang , Yan Wang
Chronic stress is a significant risk factor that contributes to the progression of colorectal cancer (CRC) and has garnered considerable attention in recent research. It influences the distribution and function of immune cells within the intestinal mucosa through the "brain-gut" axis, altering cytokine and chemokine secretion and creating an immunosuppressive tumor microenvironment. The intestine, often called the "second brain," is particularly susceptible to the effects of chronic stress. Cytokines and chemokines in intestinal mucosal immunity(IMI) are closely linked to CRC cells' proliferation, metastasis, and drug resistance under chronic stress. Recently, antidepressants have emerged as potential therapeutic agents for CRC, possibly by modulating IMI to restore homeostasis and exert anti-tumor effects. This article reviews the role of chronic stress in promoting CRC progression via its impact on intestinal mucosal immunity, explores potential targets within the intestinal mucosa under chronic stress, and proposes new approaches for CRC treatment.
慢性压力是导致结直肠癌(CRC)恶化的一个重要风险因素,在最近的研究中引起了广泛关注。它通过 "脑-肠 "轴影响肠粘膜内免疫细胞的分布和功能,改变细胞因子和趋化因子的分泌,并形成免疫抑制性肿瘤微环境。肠道常被称为 "第二大脑",特别容易受到慢性压力的影响。肠粘膜免疫中的细胞因子和趋化因子(IMI)在慢性压力下,细胞因子和趋化因子与 CRC 细胞的增殖、转移和耐药性密切相关。最近,抗抑郁药成为治疗 CRC 的潜在药物,可能是通过调节 IMI 来恢复体内平衡并发挥抗肿瘤作用。本文回顾了慢性应激通过影响肠粘膜免疫促进 CRC 进展的作用,探讨了慢性应激下肠粘膜的潜在靶点,并提出了治疗 CRC 的新方法。
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引用次数: 0
Cholecystokinin and gastrin as immune modulating hormones: Implications and applications 胆囊收缩素和胃泌素是免疫调节激素:意义和应用。
IF 9.3 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-12-01 DOI: 10.1016/j.cytogfr.2024.11.003
Gustav van Niekerk, Lara Kelchtermans, Elias Broeckhoven, Lotte Coelmont, Yeranddy A. Alpizar, Kai Dallmeier
Cholecystokinin (CCK) and gastrin are gastrointestinal hormones traditionally recognised for their roles in digestion. However, it has been recognised that these hormones may also modulate immune function. Here, we examine the immune-modulating effects of CCK and gastrin, and explore the functional significance of this dual role. In addition to the direct effect of these hormones on immune cell function, we discuss why hormones that regulate complex physiological and behavioural aspects of digestion might also influence immune responses. Notably, recent findings highlight the importance of these hormones in promoting a tolerogenic hepatic environment, particularly as the liver encounters gut-derived inflammogens following a meal. Additionally, the neuro-immune crosstalk mediated by CCK suggests that this hormone may influence immune responses indirectly via the gut-brain axis, especially in the context of infection or inflammation. Furthermore, the role of CCK in inducing feeding cessation and satiety appears to be repurposed during sickness behaviour, such as the loss of appetite during infection. Collectively, these observations suggest that nutritional strategies, including permissive underfeeding or fasting, could have important clinical implications. A deeper understanding of the dual roles of CCK and gastrin in digestion and immunity may pave the way for novel therapeutic approaches that leverage these pathways for improved disease management and treatment outcomes.
胆囊收缩素(CCK)和胃泌素是传统意义上的胃肠道激素,在消化过程中发挥作用。然而,人们已经认识到这些激素也可以调节免疫功能。在这里,我们研究了 CCK 和胃泌素的免疫调节作用,并探讨了这种双重作用的功能意义。除了这些激素对免疫细胞功能的直接影响外,我们还讨论了为什么调节消化的复杂生理和行为方面的激素也可能影响免疫反应。值得注意的是,最近的研究结果强调了这些激素在促进肝脏耐受性环境中的重要性,尤其是当肝脏在进餐后遇到来自肠道的炎症因子时。此外,CCK 介导的神经-免疫串联表明,这种激素可能会通过肠道-大脑轴间接影响免疫反应,尤其是在感染或炎症的情况下。此外,CCK 在诱导进食停止和饱腹感方面的作用似乎在疾病行为(如感染时食欲不振)中被重新利用。总之,这些观察结果表明,营养策略(包括允许性少食或禁食)可能具有重要的临床意义。更深入地了解CCK和胃泌素在消化和免疫中的双重作用,可能会为利用这些途径改善疾病管理和治疗效果的新型治疗方法铺平道路。
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引用次数: 0
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Cytokine & Growth Factor Reviews
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