Molecular Aspects of Medicine最新文献_第5页

Respiratory emerging viruses and drug resistance in lung cancer: challenges and new perspectives in treatment 呼吸道新发病毒和肺癌的耐药：治疗的挑战和新观点

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-07-15 DOI: 10.1016/j.mam.2025.101383

Qiang Wu , Wen Li , Hongli Liu , Yinyin Xue , Kaili Huang , Hossein Pourghadamyari , Zhenkun Liu

Emerging viral pathogens, particularly those targeting the respiratory system such as SARS-CoV-2 and influenza virus, pose significant challenges for patients with lung cancer. These patients show increased susceptibility to serious infections caused by these viruses as a result of immunosuppression from various therapies such as immunotherapy, chemotherapy, and targeted agents. Respiratory viral infections can induce tumor progression and drug resistance through affecting the tumor microenvironment (TME), modulating immune checkpoints, or interfering with therapeutic efficacy. The present review discusses the reciprocal interactions between these viral pathogens and lung cancer, underscoring mechanisms by which SARS-CoV-2 and influenza viruses affect the lung cancer TME promoting tumor progression, immune evasion, and ultimately, resistance to anti-cancer therapies such as tyrosine kinase inhibitors (TKIs) and immune checkpoint inhibitors (ICIs). Sections discussed in this study include: (i) increased susceptibility to viral infections, (ii) virus-induced modulation of the tumor microenvironment, and (iii) mechanisms of therapy resistance. This review also addresses emerging strategies, such as oncolytic virotherapy, as potential candidates for lung cancer treatment. It aims to provide new perspectives on therapeutic optimization for patients with lung cancer in the context of SARS-CoV-2 and influenza viruses, by reviewing evidence from virology, oncology, and immunology.

新出现的病毒病原体，特别是针对呼吸系统的病毒，如SARS-CoV-2和流感病毒，给肺癌患者带来了重大挑战。由于免疫疗法、化疗和靶向药物等各种疗法的免疫抑制，这些患者对这些病毒引起的严重感染的易感性增加。呼吸道病毒感染可通过影响肿瘤微环境（TME）、调节免疫检查点或干扰治疗效果诱导肿瘤进展和耐药。本综述讨论了这些病毒病原体与肺癌之间的相互作用，强调了SARS-CoV-2和流感病毒影响肺癌TME促进肿瘤进展、免疫逃避并最终对酪氨酸激酶抑制剂（TKIs）和免疫检查点抑制剂（ICIs）等抗癌疗法产生耐药性的机制。本研究中讨论的部分包括：(1)对病毒感染的易感性增加，(2)病毒诱导的肿瘤微环境调节，以及(3)耐药机制。本综述还讨论了新兴策略，如溶瘤病毒治疗，作为肺癌治疗的潜在候选。本研究旨在通过回顾病毒学、肿瘤学和免疫学方面的证据，为SARS-CoV-2和流感病毒背景下肺癌患者的治疗优化提供新的视角。

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引用次数: 0

Protein and RNA chaperones 蛋白质和RNA伴侣

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-07-14 DOI: 10.1016/j.mam.2025.101384

Bikash R. Sahoo, James CA. Bardwell

Cells preserve macromolecular homeostasis by utilizing molecular chaperones that prevent aggregation or promote correct folding of protein and RNA. Here we discuss non-traditional proteinaceous chaperones like RNA-binding chaperones that work by modulating RNA structure, preventing aberrant interactions, and regulating intracellular granule dynamics. We also discuss the chaperone functions of other macromolecules such as nucleic acids, and in particular G-quadruplexes, which are very effective at preventing protein aggregation and accelerating protein folding. These chaperones are particularly important in G-quadruplex linked amyloid aggregation and repeat-expansion diseases such as Parkinson's disease and amyotrophic lateral sclerosis, where RNA aggregation and misfolded protein accumulation co-occur. By comparing protein and non-protein chaperone systems, we highlight the principles that underlie chaperone action across molecular classes.

细胞通过利用分子伴侣来防止蛋白质和RNA的聚集或促进正确折叠，从而保持大分子的稳态。在这里，我们讨论非传统的蛋白质伴侣，如RNA结合伴侣，通过调节RNA结构，防止异常相互作用和调节细胞内颗粒动力学起作用。我们还讨论了其他大分子的伴侣功能，如核酸，特别是g -四联体，它在防止蛋白质聚集和加速蛋白质折叠方面非常有效。这些伴侣蛋白在g -四重体相关淀粉样蛋白聚集和重复扩张疾病（如帕金森病和肌萎缩侧索硬化症）中尤为重要，在这些疾病中，RNA聚集和错误折叠的蛋白质积累共同发生。通过比较蛋白质和非蛋白质伴侣系统，我们强调了在分子类中伴侣作用的原理。

引用次数: 0

The role of free fatty acid receptors activation in pancreatic disorders 游离脂肪酸受体激活在胰腺疾病中的作用

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-07-12 DOI: 10.1016/j.mam.2025.101386

Julia Lis, Jakub Fichna, Aleksandra Tarasiuk-Zawadzka

Free fatty acid receptors (FFARs), a subset of G protein-coupled receptors, play a pivotal role in metabolic and immune homeostasis by modulating signaling pathways in response to free fatty acids. The four main FFARs (FFAR1, FFAR2, FFAR3, and FFAR4) are especially significant in pancreatic function, regulating insulin secretion, inflammation, and glucose metabolism. These receptors are involved in key pancreatic disorders, including acute pancreatitis (AP), pancreatic cancer (PC), type 1 diabetes (T1D), and type 2 diabetes (T2D).

FFAR1, FFAR3, and FFAR4 exhibit protective effects against AP due to their anti-inflammatory properties. In PC, FFAR1 inhibits tumor cell motility, while FFAR2 downregulation may contribute to tumor progression. FFAR3 plays a role in limiting tumor proliferation, whereas FFAR4 has a dual effect, promoting metastasis while also triggering tumor cell apoptosis. In T1D, FFAR2 and FFAR4 help regulate glycemia without directly stimulating insulin secretion. In T2D, all four FFARs contribute to glycemic control and may protect pancreatic β-cells.

Despite their therapeutic potential, the precise mechanisms underlying FFAR function in pancreatic disorders remain incompletely understood. Ongoing research aims to clarify these pathways, identify optimal ligands, and assess the safety and efficacy of FFAR-targeted therapies. This growing body of evidence underscores the importance of FFARs as potential targets for innovative treatments in pancreatic diseases.

游离脂肪酸受体（FFARs）是G蛋白偶联受体的一个子集，通过调节游离脂肪酸应答的信号通路，在代谢和免疫稳态中发挥关键作用。四种主要FFARs （FFAR1、FFAR2、FFAR3和FFAR4）在胰腺功能、调节胰岛素分泌、炎症和葡萄糖代谢中尤为重要。这些受体参与关键胰腺疾病，包括急性胰腺炎（AP）、胰腺癌（PC）、1型糖尿病（T1D）和2型糖尿病（T2D）。FFAR1、FFAR3和FFAR4由于其抗炎特性对AP表现出保护作用。在PC中，FFAR1抑制肿瘤细胞运动，而FFAR2下调可能促进肿瘤进展。FFAR3发挥限制肿瘤增殖的作用，而FFAR4具有双重作用，既促进肿瘤转移，又触发肿瘤细胞凋亡。在T1D中，FFAR2和FFAR4在不直接刺激胰岛素分泌的情况下帮助调节血糖。在T2D中，所有四种ffar都有助于血糖控制，并可能保护胰腺β细胞。尽管具有治疗潜力，但FFAR在胰腺疾病中功能的确切机制仍不完全清楚。正在进行的研究旨在阐明这些途径，确定最佳配体，并评估ffar靶向治疗的安全性和有效性。越来越多的证据强调了FFARs作为胰腺疾病创新治疗的潜在靶点的重要性。

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引用次数: 0

Ischemia - Reperfusion injury: A roadmap to precision therapies 缺血-再灌注损伤：精确治疗的路线图

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-07-08 DOI: 10.1016/j.mam.2025.101382

Wei Li , Yan Liao , Jie Chen , Weichao Kang , Xintao Wang , Xiaozhu Zhai , Ying Xue , Wangzheqi Zhang , Yiyang Xia , Derong Cui

Ischemia-reperfusion (I/R) injury is prevalent in the medical field and significantly limits the therapeutic outcomes of various ischemic diseases, adversely affecting patient prognosis. The pathogenesis of I/R injury is highly complex, involving intricate interactions among oxidative stress, inflammatory responses, mitochondrial dysfunction, and multiple cell death pathways. Once the mitochondrial respiratory chain is impaired, it triggers oxidative stress responses, leading to the excessive production of reactive oxygen species (ROS). Excessive ROS not only directly damage cells but also activate inflammatory responses and initiate multiple cell death signalling pathways, such as necroptosis, pyroptosis, and ferroptosis, thereby exacerbating tissue damage. Moreover, the clinical manifestations of I/R injury vary significantly across different organs, such as the heart, brain, kidneys, liver, and lungs, and are further influenced by patients' underlying conditions, posing challenges for clinical diagnosis and treatment. Therefore, constructing a comprehensive assessment system based on individual patient characteristics (such as genetic polymorphisms and comorbidities) to accurately predict the risk of I/R injury is particularly important. Currently, there are diverse strategies for the prevention and treatment of I/R injury, but translating basic research into clinical application remains challenging. Developing personalized treatment plans tailored to different cell types holds promise for overcoming existing therapeutic bottlenecks, significantly improving patient outcomes, and providing new directions for addressing the challenges of I/R injury.

缺血再灌注（I/R）损伤在医学领域普遍存在，严重限制了各种缺血性疾病的治疗效果，对患者预后产生不利影响。I/R损伤的发病机制非常复杂，涉及氧化应激、炎症反应、线粒体功能障碍和多种细胞死亡途径之间复杂的相互作用。一旦线粒体呼吸链受损，就会引发氧化应激反应，导致活性氧（ROS）的过量产生。过多的ROS不仅会直接损伤细胞，还会激活炎症反应，启动多种细胞死亡信号通路，如坏死、焦亡、铁亡等，从而加重组织损伤。此外，I/R损伤的临床表现在心、脑、肾、肝、肺等不同器官之间存在显著差异，并进一步受到患者基础疾病的影响，给临床诊断和治疗带来挑战。因此，构建基于患者个体特征（如遗传多态性、合并症等）的综合评估体系，准确预测I/R损伤风险就显得尤为重要。目前，预防和治疗I/R损伤的策略多种多样，但将基础研究转化为临床应用仍然具有挑战性。开发针对不同细胞类型的个性化治疗方案有望克服现有的治疗瓶颈，显著改善患者的预后，并为解决I/R损伤的挑战提供新的方向。

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引用次数: 0

Type 2 Diabetes Mellitus and bladder cancer: A narrative review on associated signaling pathways 2型糖尿病和膀胱癌：相关信号通路的叙述综述

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-06-20 DOI: 10.1016/j.mam.2025.101381

Lívia da Cunha Agostini, Glenda Nicioli da Silva

Bladder cancer is one of the most common cancers globally. The risk factors for urothelial bladder cancer can be broadly divided into genetic predispositions and external environmental exposures. Type 2 Diabetes Mellitus (T2DM) is a chronic, non-communicable metabolic disorder, and the interaction between genetic, behavioral, and environmental factors plays a significant role in its development. The management of T2DM includes lifestyle modifications and medication. Several studies suggest that T2DM is associated with an increased risk of bladder cancer. This review highlights the key signaling mechanisms involved in this association and explores the impact of T2DM medications on bladder cancer. In conclusion, the literature suggests that metabolic abnormalities associated with T2DM —such as hyperglycemia, insulin resistance and elevated levels of insulin, insulin-like growth factor 1 (IGF-1), inflammatory cytokines, iNOS/eNOS activity, hypoxia, dyslipidemia, matrix metalloproteinase (MMPs), leptin, vimentin, N-cadherin, fibronectin, advanced glycation end products (AGEs), endoplasmic reticulum stress (ERS), and Arntl2 gene expression; in addition to reduced E-cadherin, adiponectin, autophagy, and IGF-1 and Usp2 gene expression—significantly influence signaling pathways essential for bladder tumor development. Additionally, the choice of hypoglycemic treatment should be carefully considered, taking into account potential effects on carcinogenesis.

膀胱癌是全球最常见的癌症之一。尿路上皮性膀胱癌的危险因素大致可分为遗传易感性和外部环境暴露。2型糖尿病（T2DM）是一种慢性非传染性代谢性疾病，遗传、行为和环境因素的相互作用在其发病过程中起着重要作用。T2DM的管理包括生活方式的改变和药物治疗。一些研究表明，2型糖尿病与膀胱癌风险增加有关。这篇综述强调了这种关联的关键信号机制，并探讨了T2DM药物对膀胱癌的影响。总之，文献提示与T2DM相关的代谢异常，如高血糖、胰岛素抵抗和胰岛素水平升高、胰岛素样生长因子1 （IGF-1）、炎症因子、iNOS/eNOS活性、缺氧、血脂异常、基质金属蛋白酶（MMPs）、瘦素、vimentin、n-钙粘蛋白、纤维连接蛋白、晚期糖基化终产物（AGEs）、内质网应激（ERS）和Arntl2基因表达；除了e -钙粘蛋白、脂联素、自噬、IGF-1和Usp2基因表达减少外，还显著影响膀胱肿瘤发展所必需的信号通路。此外，应仔细考虑降糖治疗的选择，考虑到潜在的致癌作用。

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引用次数: 0

Cardiovascular impact of emerging and Re-emerging Viruses: Pathophysiological mechanisms, diagnosis, and management with a pediatric focus 新出现的和再出现的病毒对心血管的影响：病理生理机制、诊断和管理，以儿科为重点

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-05-26 DOI: 10.1016/j.mam.2025.101371

Li Li , Xu Shi , Ruiming Wang , Yuxi Fan , Zhihan Xu , Habibollah Mirzaei , Wuran Wei

Emerging and re-emerging viruses are currently known as a major public health issue. These viruses can cause various human complications such as cardiovascular diseases (CVDs), both in adults and pediatric populations. Although various CVDs have been previously reported for emerging and re-emerging viruses, the mechanisms underlying these complications remain relatively unknown. Children and infants, while commonly developing less severe symptoms, may experience notable cardiovascular manifestations during infections caused by emerging and re-emerging viral infections, which can result in both acute and long-term complications. The present review aims to discuss various cardiovascular complications linked to emerging and re-emerging viral pathogens (including severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), dengue virus (DENV), Zika virus (ZIKV), and chikungunya virus (CHIKV)) such as arrhythmias, myocarditis, vascular disorders, and thromboembolic conditions, particularly among the pediatric population. This review also addresses the potential mechanisms by which SARS-CoV-2, DENV, ZIKV, and CHIKV may impact the cardiovascular system and their clinical implications. Moreover, it discusses the diagnostic challenges for viral-caused cardiovascular disorders in children, owing to their common subtle or atypical manifestations. Finally, it addresses the present therapeutic specifically used for pediatric cases.

新出现和再出现的病毒目前被认为是一个重大的公共卫生问题。这些病毒可在成人和儿童人群中引起各种人类并发症，如心血管疾病（cvd）。虽然以前已经报道了新出现和再出现的病毒引起的各种心血管疾病，但这些并发症的机制仍然相对未知。儿童和婴儿虽然通常出现不太严重的症状，但在新发和再发病毒感染引起的感染期间可能出现明显的心血管症状，这可能导致急性和长期并发症。本综述旨在讨论与新出现和再出现的病毒性病原体（包括严重急性呼吸综合征冠状病毒2 （SARS-CoV-2）、登革热病毒（DENV）、寨卡病毒（ZIKV）和基孔肯雅病毒（CHIKV））相关的各种心血管并发症，如心律失常、心肌炎、血管疾病和血栓栓塞性疾病，特别是在儿科人群中。本综述还探讨了SARS-CoV-2、DENV、ZIKV和CHIKV可能影响心血管系统的潜在机制及其临床意义。此外，它讨论了诊断挑战的病毒引起的心血管疾病的儿童，由于他们的共同微妙或非典型的表现。最后，它解决了目前治疗专门用于儿科病例。

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引用次数: 0

Adiponectin: its role in diabetic and pancreatic cancer 脂联素在糖尿病和胰腺癌中的作用

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-05-21 DOI: 10.1016/j.mam.2025.101370

Seema Kumari , Sujatha Peela , Mundla Srilatha , Bala Prabhakar Girish , Ganji Purnachandra Nagaraju

Adiponectin (ApN) is an antidiabetic and anti-inflammatory protein synthesized by adipose tissue. It is essential in regulating insulin sensitivity, glucose, and lipid metabolism by controlling AMPK, PPARα, and MAPK signals. It is an anti-inflammatory property that protects pancreatic β-cells. Often, low levels of ApN are linked to obesity, type II diabetes and the development of PDAC. However, changes in lifestyle and the use of certain drugs can improve ApN function and insulin sensitivity. PDAC is a highly aggressive cancer linked to obesity, type II diabetes, and insulin resistance. ApN plays a complex role in PDAC progression and can suppress PDAC development by weakening β-catenin signaling. Decreases in ApN levels are associated with increased PDAC risk in diabetic patients. PDAC and diabetes are interconnected through the development of insulin resistance, islet dysfunction, change in immunological response, inflammation, oxidative stress, and altered hormone secretion. Genetic studies highlight specific genes like HNF4G and PDX1 that influence both conditions and miRNAs such as miR-19a promote tumor progression through the PI3K/AKT pathway. This review discusses the role of ApN in diabetes and PDAC and the interrelation between diabetes and PDAC.

脂联素（Adiponectin, ApN）是一种由脂肪组织合成的抗糖尿病和抗炎蛋白。它通过控制AMPK、PPARα和MAPK信号来调节胰岛素敏感性、葡萄糖和脂质代谢。它具有抗炎特性，可以保护胰腺β细胞。通常，低水平的ApN与肥胖、II型糖尿病和PDAC的发展有关。然而，生活方式的改变和某些药物的使用可以改善ApN功能和胰岛素敏感性。PDAC是一种高度侵袭性的癌症，与肥胖、II型糖尿病和胰岛素抵抗有关。ApN在PDAC的发展过程中发挥着复杂的作用，可以通过削弱β-catenin信号传导抑制PDAC的发展。糖尿病患者ApN水平降低与PDAC风险增加相关。PDAC和糖尿病通过胰岛素抵抗、胰岛功能障碍、免疫反应改变、炎症、氧化应激和激素分泌改变而相互关联。遗传学研究强调了HNF4G和PDX1等特定基因对两种疾病都有影响，而miR-19a等mirna通过PI3K/AKT通路促进肿瘤进展。本文就ApN在糖尿病和PDAC中的作用以及糖尿病与PDAC的相互关系作一综述。

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引用次数: 0

Virus-like particles of retroviral origin in protein aggregation and neurodegenerative diseases 蛋白质聚集和神经退行性疾病中源自逆转录病毒的病毒样颗粒

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-05-20 DOI: 10.1016/j.mam.2025.101369

Serena Carra , Balazs Fabian , Hamed Taghavi , Edoardo Milanetti , Valeria Giliberti , Giancarlo Ruocco , Jason Shepherd , Michele Vendruscolo , Monika Fuxreiter

A wide range of human diseases are associated with protein misfolding and amyloid aggregates. Recent studies suggest that in certain neurological disorders, including Amyotrophic Lateral Sclerosis (ALS), Frontotemporal Dementia (FTD) and various tauopathies, protein aggregation may be promoted by virus-like particles (VLPs) formed by endogenous retroviruses (ERVs). The molecular mechanisms by which these VLPs contribute to protein aggregation, however, remain enigmatic. Here, we discuss possible molecular mechanisms of ERV-derived VLPs in the formation and spread of protein aggregates. An intriguing possibility is that liquid-like condensates may facilitate the formation of both protein aggregates and ERV-derived VLPs. We also describe how RNA chaperoning, and the encapsulation and trafficking of misfolded proteins, may contribute to protein homeostasis through the elimination of protein aggregates from cells. Based on these insights, we discuss future potential therapeutic opportunities.

许多人类疾病都与蛋白质错误折叠和淀粉样蛋白聚集有关。最近的研究表明，在某些神经系统疾病中，包括肌萎缩侧索硬化症（ALS）、额颞叶痴呆（FTD）和各种牛头病，内源性逆转录病毒（erv）形成的病毒样颗粒（vlp）可能促进蛋白质聚集。然而，这些VLPs促进蛋白质聚集的分子机制仍然是谜。在这里，我们讨论了erv衍生的VLPs在蛋白质聚集体形成和扩散中的可能分子机制。一种有趣的可能性是，液体状凝聚物可能促进蛋白质聚集体和erv衍生的VLPs的形成。我们还描述了RNA陪伴，以及错误折叠蛋白质的封装和运输，如何通过消除细胞中的蛋白质聚集体来促进蛋白质稳态。基于这些见解，我们讨论了未来潜在的治疗机会。

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引用次数: 0

Metabolic reprogramming of drug resistance in pancreatic cancer: mechanisms and effects 胰腺癌耐药的代谢重编程：机制和影响

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-05-20 DOI: 10.1016/j.mam.2025.101368

Jinyi Zhang , Xueqing Kong , Boyan Zhou , Rui Li , Zhaoan Yu , Jinrong Zhu , Qing Xi , Yan Li , Zichao Zhao , Rongxin Zhang

Pancreatic cancer is a highly aggressive gastrointestinal malignancy, often termed the “king of cancers” due to its notoriously high mortality rate. Its clinical characteristics, including late diagnosis, low surgical resectability, high recurrence rates, significant chemoresistance, and poor prognosis have collectively driven the persistent rise in incidence and mortality. Despite ongoing advancements in therapeutic strategies, the management of pancreatic cancer, particularly at advanced stages, remains challenging. Chemotherapy remains the mainstay of current treatment. However, the prevalent problem of chemotherapy resistance poses a significant obstacle to effective treatment. Metabolic reprogramming, characterized by alterations in glucose metabolism, lipid biosynthesis, and amino acid utilization, supports the high energy demands and rapid proliferation of cancer cells. Emerging evidence suggests that these metabolic changes, possibly mediated by epigenetic mechanisms, also contribute to tumorigenesis and metastasis. These findings highlight the critical role of metabolic alterations in pancreatic cancer pathogenesis. This review explores the relationship between metabolic reprogramming and chemotherapy resistance, discussing underlying mechanisms and summarizing preclinical studies and drug development targeting metabolism. The aim is to provide a comprehensive perspective on potential therapeutic strategies for pancreatic cancer.

胰腺癌是一种高度侵袭性的胃肠道恶性肿瘤，由于其众所周知的高死亡率，常被称为“癌症之王”。其临床特点，包括诊断晚，手术可切除性低，复发率高，化疗耐药明显，预后差，共同推动发病率和死亡率持续上升。尽管治疗策略不断进步，但胰腺癌的管理，特别是在晚期，仍然具有挑战性。化疗仍然是目前治疗的主要方法。然而，普遍存在的化疗耐药问题对有效治疗构成了重大障碍。代谢重编程以葡萄糖代谢、脂质生物合成和氨基酸利用的改变为特征，支持癌细胞的高能量需求和快速增殖。新的证据表明，这些代谢变化，可能是由表观遗传机制介导的，也有助于肿瘤的发生和转移。这些发现强调了代谢改变在胰腺癌发病机制中的关键作用。本文综述了代谢重编程与化疗耐药之间的关系，讨论了其潜在机制，并总结了针对代谢的临床前研究和药物开发。目的是为胰腺癌的潜在治疗策略提供一个全面的视角。

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引用次数: 0

Recent advances in the diagnosis of fungal zoonoses in India: A comprehensive overview 印度真菌性人畜共患病诊断的最新进展：全面概述

IF 8.7 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Molecular Aspects of Medicine

Pub Date : 2025-05-09 DOI: 10.1016/j.mam.2025.101366

Pradeep J , P. Lavanya , Mashila A , Naveen Kumar C

Fungal infections are most common in integumentary and systemic parts of the body. The outbreak of fungal infections was observed in several disease conditions like Pulmonary tuberculosis (PTB), chronic obstructive disease (COPD), malignancies and others like COVID-19 associated Mucormycosis (Black fungus) among Indian population. The main objective of the study is to examine the recent advanced techniques available in India for the diagnosis of fungal infections. We conclude that the study has mainly focuses on the recent advances on the diagnosis of fungal infections in India. The prevalence of zoonotic fungal infections among humans is alarming, and global health is moving towards the existence of a one-health approach.

真菌感染最常见于身体的表皮和全身部位。在印度人口中，在肺结核（PTB）、慢性阻塞性疾病（COPD）、恶性肿瘤和其他疾病（如COVID-19相关的毛霉菌病（黑真菌））等几种疾病中观察到真菌感染的爆发。该研究的主要目的是检查印度用于真菌感染诊断的最新先进技术。我们的结论是，研究主要集中在真菌感染的诊断在印度的最新进展。人类人畜共患真菌感染的流行程度令人震惊，全球卫生正朝着单一健康方法的方向发展。

引用次数: 0