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The dual role of the TSC complex in cancer. TSC 复合物在癌症中的双重作用。
IF 12.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 DOI: 10.1016/j.molmed.2024.10.009
Josephine Hartung, Christine Müller, Cornelis F Calkhoven

The tuberous sclerosis complex (TSC1/TSC2/TBC1D7) primarily functions to inhibit the mechanistic target of rapamycin complex 1 (mTORC1), a crucial regulator of cell growth. Mutations in TSC1 or TSC2 cause tuberous sclerosis complex (TSC), a rare autosomal dominant genetic disorder marked by benign tumors in multiple organs that rarely progress to malignancy. Traditionally, TSC proteins are considered tumor suppressive due to their inhibition of mTORC1 and other mechanisms. However, more recent studies have shown that TSC proteins can also promote tumorigenesis in certain cancer types. In this review, we explore the composition and function of the TSC protein complex, the roles of its individual components in cancer biology, and potential future therapeutic targeting strategies.

结节性硬化症复合体(TSC1/TSC2/TBC1D7)的主要功能是抑制雷帕霉素复合体 1(mTORC1)的机制靶标,这是细胞生长的一个重要调节因子。TSC1 或 TSC2 基因突变会导致结节性硬化综合征(TSC),这是一种罕见的常染色体显性遗传疾病,其特征是在多个器官中出现良性肿瘤,但很少发展为恶性肿瘤。传统上,TSC 蛋白由于抑制 mTORC1 和其他机制而被认为具有抑制肿瘤的作用。然而,最近的研究表明,TSC 蛋白也能促进某些癌症类型的肿瘤发生。在这篇综述中,我们将探讨 TSC 蛋白复合物的组成和功能、其各个成分在癌症生物学中的作用以及未来潜在的靶向治疗策略。
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引用次数: 0
The aging lipidome: exercise is medicine. 衰老的脂质体:运动就是药物。
IF 12.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-06-24 DOI: 10.1016/j.molmed.2024.06.006
Abel Plaza-Florido, Inmaculada Pérez-Prieto, Alejandro Lucia

The molecular mechanisms behind the potential 'anti-aging' effects of exercise remain to be elucidated. Janssens et al. studied the lipidome of different mouse tissues and human skeletal muscle. They identified an evolutionary conserved 'lipid aging' signature, characterized by bis(monoacylglycero)phosphate accumulation, which, at the muscle level, can be attenuated by exercise.

运动潜在 "抗衰老 "作用背后的分子机制仍有待阐明。Janssens 等人研究了不同小鼠组织和人类骨骼肌的脂质体。他们发现了一种进化保守的 "脂质老化 "特征,其特点是双(单酰基甘油)磷酸酯的积累,在肌肉水平上,运动可减轻这种积累。
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引用次数: 0
Amyloid and collagen templates in aortic valve calcification. 主动脉瓣钙化中的淀粉样蛋白和胶原蛋白模板。
IF 12.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-06-05 DOI: 10.1016/j.molmed.2024.04.015
Shobini Jayaraman, Navneet Narula, Jagat Narula, Olga Gursky

Calcific aortic valve disease (CAVD) is a widely prevalent heart disorder in need of pharmacological interventions. Calcified areas in aortic valves often contain amyloid fibrils that promote calcification in vitro. This opinion paper suggests that amyloid contributes to CAVD development; amyloid-assisted nucleation can accelerate hydroxyapatite deposition onto collagen matrix. Notably, acidic arrays in amyloid match calcium-calcium spacing in the amorphous hydroxyapatite precursor, while oscillating hemodynamic perturbations promote amyloid deposition in the valve. Lipoprotein(a), a genetic risk factor for CAVD, augments calcification via several mechanisms, wherein hydrolysis of oxidized phospholipids (oxPLs) by Lp(a)-associated enzymes helps generate orthophosphate, and apolipoprotein(a) blocks plasmin-induced fibril degradation. Current studies of amyloid-calcium-collagen interactions in solution and in fibrillar complexes allow deeper insight into the role of amyloid in calcification.

主动脉瓣钙化病(CAVD)是一种广泛流行的心脏疾病,需要药物干预。主动脉瓣的钙化区通常含有淀粉样纤维,可促进体外钙化。这篇论文认为,淀粉样蛋白有助于CAVD的发展;淀粉样蛋白辅助成核可加速羟基磷灰石在胶原基质上的沉积。值得注意的是,淀粉样蛋白中的酸性阵列与无定形羟基磷灰石前体中的钙-钙间距相匹配,而振荡的血流动力学扰动会促进淀粉样蛋白在瓣膜中的沉积。脂蛋白(a)是心血管疾病的遗传风险因素,它通过几种机制促进钙化,其中脂蛋白(a)相关酶水解氧化磷脂(oxPLs)有助于生成正磷酸盐,而脂蛋白(a)则会阻止浆蛋白诱导的纤维降解。目前对溶液中和纤维状复合物中淀粉样蛋白-钙-胶原蛋白相互作用的研究有助于深入了解淀粉样蛋白在钙化中的作用。
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引用次数: 0
Unraveling host genetics and microbiome genome crosstalk: a novel therapeutic approach. 揭示宿主遗传学和微生物组基因组串扰:一种新的治疗方法。
IF 12.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-06-27 DOI: 10.1016/j.molmed.2024.06.007
Qian Zhang, Dennis Schwarz, Yumei Cheng, Yahya Sohrabi

The ability of the gut microbiome to adapt to a new environment and utilize a new metabolite or dietary compound by inducing structural variations (SVs) in the genome has an important role in human health. Here, we discuss recent data on host genetic regulation of SV induction and its use as a new therapeutic approach.

肠道微生物组通过诱导基因组中的结构变异(SV)来适应新环境并利用新的代谢物或膳食化合物的能力对人类健康具有重要作用。在此,我们将讨论有关诱导 SV 的宿主基因调控及其作为一种新的治疗方法的最新数据。
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引用次数: 0
Cognitive impairment in people living with HIV: mechanisms, controversies, and future perspectives. 艾滋病病毒感染者的认知障碍:机制、争议和未来展望。
IF 12.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-07-01 DOI: 10.1016/j.molmed.2024.06.005
Charalampos D Moschopoulos, Kate Alford, Anastasia Antoniadou, Jaime H Vera

Despite the dramatic decrease in HIV-associated neurocognitive impairment (NCI) in the combined antiretroviral treatment (cART) era, subtler neuropsychological complications remain prevalent. In this review, we discuss the changing pathophysiology of HIV-associated NCI, considering recent evidence of HIV neuropathogenesis, and the pivotal role of cART. Furthermore, we address the multifactorial nature of NCI in people living with HIV, including legacy and ongoing insults to the brain, as well as host-specific factors. We also summarize the ongoing debate about the refinement of diagnostic criteria, exploring the strengths and limitations of these recent approaches. Finally, we present current research in NCI management in people living with HIV and highlight the need for using both pharmacological and nonpharmacological pathways toward a holistic approach.

尽管在联合抗逆转录病毒治疗(cART)时代,HIV 相关神经认知障碍(NCI)急剧下降,但更微妙的神经心理并发症仍然普遍存在。在这篇综述中,我们讨论了 HIV 相关神经认知障碍不断变化的病理生理学,考虑了 HIV 神经发病机制的最新证据,以及 cART 的关键作用。此外,我们还讨论了 HIV 感染者 NCI 的多因素性质,包括对大脑的遗留和持续损伤,以及宿主特异性因素。我们还总结了目前关于完善诊断标准的争论,探讨了这些最新方法的优势和局限性。最后,我们介绍了目前对艾滋病病毒感染者进行 NCI 管理的研究情况,并强调有必要同时使用药物和非药物方法来实现综合治疗。
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引用次数: 0
Fc-optimized checkpoint antibodies for cancer immunotherapy. 用于癌症免疫疗法的 Fc 优化检查点抗体。
IF 12.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 DOI: 10.1016/j.molmed.2024.10.008
Rony Dahan, Alan J Korman

The development of checkpoint antibodies for cancer therapy has been guided by the principle of blocking T cell inhibitory signals. Recognition of the role of the Fc domain in therapeutic activities, through the depletion of immunosuppressive populations and myeloid cell activation, prompts a shift toward the development of optimized Fc-engineered checkpoint antibodies.

用于癌症治疗的检查点抗体的开发一直遵循阻断 T 细胞抑制信号的原则。人们认识到 Fc 结构域通过消耗免疫抑制群体和激活髓系细胞在治疗活动中的作用,这促使人们转向开发优化的 Fc 工程检查点抗体。
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引用次数: 0
Virus as the cause of type 1 diabetes. 病毒是 1 型糖尿病的病因。
IF 12.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-11-01 Epub Date: 2024-07-13 DOI: 10.1016/j.molmed.2024.06.011
Knut Dahl-Jørgensen

Type 1 diabetes (T1D), a severe disease requiring intensive insulin treatment, carries an increased risk for complications and reduced lifespan. Certain viruses have been implicated in T1D's etiology, with 'live', replicating enteroviruses (EVs) recently found in the pancreas at diagnosis. This discovery prompted a trial to slow down disease progression using antiviral drugs. A 6-month treatment combining pleconaril and ribavirin in new-onset T1D patients preserved residual insulin production after 1 year, unlike placebo. The results support the theory that viruses may cause T1D in genetically susceptible individuals. A low-grade, persistent viral infection may initiate a cascade of pathogenic mechanisms initially involving the innate immune system, inducing β-cell stress and neoantigen release, leading to autoimmunity, and eventually the destruction of insulin-producing β-cells.

1 型糖尿病(T1D)是一种需要大量胰岛素治疗的严重疾病,并发症风险增加,寿命缩短。某些病毒与 T1D 的病因有关,最近在诊断时在胰腺中发现了 "活 "的、可复制的肠道病毒 (EV)。这一发现推动了一项使用抗病毒药物延缓疾病进展的试验。与安慰剂不同的是,对新发 T1D 患者进行的为期 6 个月的 pleconaril 和利巴韦林联合治疗在 1 年后仍能保留残余的胰岛素分泌。这些结果支持了病毒可能导致基因易感者患上 T1D 的理论。低度、持续的病毒感染可能会启动一连串的致病机制,最初涉及先天性免疫系统,诱发β细胞应激和新抗原释放,导致自身免疫,最终破坏产生胰岛素的β细胞。
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引用次数: 0
Science around the world. 世界各地的科学
IF 12.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-29 DOI: 10.1016/j.molmed.2024.09.007
Abel Plaza-Florido, Olga Gursky, Macarena Lorena Herrera, Charalampos D Moschopoulos, Yahya Sohrabi
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引用次数: 0
Advances in Hodgkin lymphoma research. 霍奇金淋巴瘤研究进展。
IF 12.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-22 DOI: 10.1016/j.molmed.2024.10.004
Ralf Küppers

Hodgkin lymphoma (HL) has been and still is the most enigmatic lymphoid malignancy in humans. Since the first molecular analysis of isolated Hodgkin and Reed-Sternberg (HRS) tumor cells of classic HL 30 years ago, substantial advances in our understanding of HL have been made. This review describes the cellular origin of HL, summarizes the current knowledge about the genetic lesions in HRS cells, and highlights the role of Epstein-Barr virus (EBV) in HL pathogenesis. Moreover, the pathobiological roles of altered gene expression and deregulated signaling pathways are discussed and key aspects of the HL microenvironment are presented.

霍奇金淋巴瘤(HL)过去是,现在仍然是人类最神秘的淋巴恶性肿瘤。自 30 年前首次对典型 HL 的分离霍奇金和里德-斯特恩伯格(HRS)肿瘤细胞进行分子分析以来,我们对 HL 的认识取得了重大进展。这篇综述描述了 HL 的细胞起源,总结了目前有关 HRS 细胞遗传病变的知识,并强调了 Epstein-Barr 病毒(EBV)在 HL 发病机制中的作用。此外,还讨论了基因表达改变和信号通路失调的病理生物学作用,并介绍了 HL 微环境的主要方面。
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引用次数: 0
Targeting monoamine oxidases in cancer: advances and opportunities. 以癌症中的单胺氧化酶为靶点:进展与机遇。
IF 12.8 1区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2024-10-21 DOI: 10.1016/j.molmed.2024.09.010
Jing Wei, Boyang Jason Wu

Monoamine oxidases (MAOs) are a crucial pair of isoenzymes responsible for degrading monoamine neurotransmitters and dietary amines. In addition to extensive studies of their roles in the context of brain functions and disorders over decades, emerging evidence indicates that MAOs are also often dysregulated and associated with clinical outcomes in diverse cancers, with the ability to differentially regulate cancer growth, invasion, metastasis, progression, and therapy response depending on the cancer type. In this review, we summarize recent advances in understanding the clinical relevance, functional importance, and mechanisms of MAOs in a broad range of cancers, and discuss the application and therapeutic benefit of MAO inhibitors (MAOIs) for cancer treatment, highlighting the roles of MAOs as novel regulators, prognostic biomarkers, and therapeutic targets in cancer.

单胺氧化酶(MAOs)是一对重要的同工酶,负责降解单胺神经递质和膳食胺。几十年来,除了对其在大脑功能和失调方面的作用进行广泛研究外,新出现的证据表明,MAOs 也经常失调,并与各种癌症的临床结果相关,能够根据癌症类型的不同而对癌症的生长、侵袭、转移、进展和治疗反应进行不同程度的调节。在这篇综述中,我们总结了最近在理解MAOs在多种癌症中的临床相关性、功能重要性和机制方面取得的进展,并讨论了MAO抑制剂(MAOIs)在癌症治疗中的应用和治疗效果,强调了MAOs在癌症中作为新型调节剂、预后生物标志物和治疗靶点的作用。
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Trends in molecular medicine
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