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TGF-β mediated drug resistance in solid cancer TGF-β介导的实体癌耐药
IF 13 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.04.001
Marta Turati , Alexandra Mousset , Nervana Issa , Andrei Turtoi , Roberto Ronca

Transforming growth factor β (TGF-β) is an important signaling molecule which is expressed in three different isoforms in mammals (i.e. TGF-β1, -β2, and -β3). The interaction between TGF-β and its receptor triggers several pathways, which are classified into SMAD-dependent (canonical) and SMAD-independent (non-canonical) signaling, whose activation/transduction is finely regulated by several mechanisms. TGF-β is involved in many physiological and pathological processes, assuming a dualistic role in cancer progression depending on tumor stage. Indeed, TGF-β inhibits cell proliferation in early-stage tumor cells, while it promotes cancer progression and invasion in advanced tumors, where high levels of TGF-β have been reported in both tumor and stromal cells. In particular, TGF-β signaling has been found to be strongly activated in cancers after treatment with chemotherapeutic agents and radiotherapy, resulting in the onset of drug resistance conditions. In this review we provide an up-to-date description of several mechanisms involved in TGF-β-mediated drug resistance, and we report different strategies that are currently under development in order to target TGF-β pathway and increase tumor sensitivity to therapy.

转化生长因子β(TGF-β)是一种重要的信号分子,在哺乳动物中以三种不同的亚型表达(即TGF-β1、-β2和-β3)。TGF-β与其受体之间的相互作用触发了几种途径,分为SMAD依赖性(经典)和SMAD非依赖性(非经典)信号传导,其激活/转导受到多种机制的精细调节。TGF-β参与许多生理和病理过程,根据肿瘤分期在癌症进展中扮演双重角色。事实上,TGF-β抑制早期肿瘤细胞的细胞增殖,同时促进晚期肿瘤中癌症的进展和侵袭,据报道,肿瘤和基质细胞中都存在高水平的TGF-β。特别是,已经发现TGF-β信号在癌症中在化疗药物和放疗后被强烈激活,导致耐药性的发作。在这篇综述中,我们对TGF-β介导的耐药性的几种机制进行了最新的描述,并报道了目前正在开发的不同策略,以靶向TGF-β途径并提高肿瘤对治疗的敏感性。
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引用次数: 7
Brain-derived neurotrophic factor: Its role in energy balance and cancer cachexia 脑源性神经营养因子:在能量平衡和癌症恶病质中的作用
IF 13 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.07.003
Barış Çerçi , Ayşenur Gök , Aytekin Akyol

Brain-derived neurotrophic factor (BDNF) plays an important role in the development of the central and peripheral nervous system during embryogenesis. In the mature central nervous system, BDNF is required for the maintenance and enhancement of synaptic transmissions and the survival of neurons. Particularly, it is involved in the modulation of neurocircuits that control energy balance through food intake, energy expenditure, and locomotion. Regulation of BDNF in the central nervous system is complex and environmental factors affect its expression in murine models which may reflect to phenotype dramatically. Furthermore, BDNF and its high-affinity receptor tropomyosin receptor kinase B (TrkB), as well as pan-neurotrophin receptor (p75NTR) is expressed in peripheral tissues in adulthood and their signaling is associated with regulation of energy balance. BDNF/TrkB signaling is exploited by cancer cells as well and BDNF expression is increased in tumors. Intriguingly, previously demonstrated roles of BDNF in regulation of food intake, adipose tissue and muscle overlap with derangements observed in cancer cachexia. However, data about the involvement of BDNF in cachectic cancer patients and murine models are scarce and inconclusive. In the future, knock-in and/or knock-out experiments with murine cancer models could be helpful to explore potential new roles for BDNF in the development of cancer cachexia.

脑源性神经营养因子(BDNF)在胚胎发生过程中对中枢和外周神经系统的发育起着重要作用。在成熟的中枢神经系统中,BDNF是维持和增强突触传递以及神经元存活所必需的。特别是,它参与调节神经回路,通过食物摄入、能量消耗和运动来控制能量平衡。BDNF在中枢神经系统中的调节是复杂的,环境因素影响其在小鼠模型中的表达,这可能会显著反映表型。此外,BDNF及其高亲和力受体原肌球蛋白受体激酶B(TrkB)以及泛神经营养因子受体(p75NTR)在成年期的外周组织中表达,其信号传导与能量平衡的调节有关。BDNF/TrkB信号传导也被癌症细胞利用,并且BDNF在肿瘤中的表达增加。有趣的是,先前证实的BDNF在食物摄入、脂肪组织和肌肉调节中的作用与癌症恶病质中观察到的失调重叠。然而,关于BDNF在恶病质癌症患者和小鼠模型中的参与的数据很少且不确定。未来,小鼠癌症模型的敲除和/或敲除实验可能有助于探索BDNF在癌症恶病质发展中的潜在新作用。
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引用次数: 0
Growth differentiation factor 11: A new hope for the treatment of cardiovascular diseases 生长分化因子11:治疗心血管疾病的新希望
IF 13 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.06.007
Yingchun Shao , Yanhong Wang , Jiazhen Xu , Yang Yuan , Dongming Xing

Growth differentiation factor 11 (GDF11) is a member of the transforming growth factor-β superfamily that has garnered significant attention due to its anti-cardiac aging properties. Many studies have revealed that GDF11 plays an indispensable role in the onset of cardiovascular diseases (CVDs). Consequently, it has emerged as a potential target and novel therapeutic agent for CVD treatment. However, currently, no literature reviews comprehensively summarize the research on GDF11 in the context of CVDs. Therefore, herein, we comprehensively described GDF11’s structure, function, and signaling in various tissues. Furthermore, we focused on the latest findings concerning its involvement in CVD development and its potential for clinical translation as a CVD treatment. We aim to provide a theoretical basis for the prospects and future research directions of the GDF11 application regarding CVDs.

生长分化因子11(GDF11)是转化生长因子-β超家族的一员,由于其抗心脏衰老的特性而受到广泛关注。许多研究表明,GDF11在心血管疾病(CVD)的发病中起着不可或缺的作用。因此,它已成为CVD治疗的潜在靶点和新型治疗剂。然而,目前没有文献综述全面总结CVDs背景下对GDF11的研究。因此,在本文中,我们全面描述了GDF11在各种组织中的结构、功能和信号传导。此外,我们重点关注了有关其参与CVD发展的最新发现,以及其作为CVD治疗的临床转化潜力。我们的目的是为GDF11在心血管疾病方面的应用前景和未来的研究方向提供理论依据。
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引用次数: 0
Recent progress and prospects for anti-cytokine therapy in preclinical and clinical acute lung injury 抗细胞因子治疗临床前和临床急性肺损伤的研究进展及展望
IF 13 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.07.002
Guilherme Pasetto Fadanni , João Batista Calixto

Acute respiratory distress syndrome (ARDS) is a heterogeneous cause of respiratory failure that has a rapid onset, a high mortality rate, and for which there is no effective pharmacological treatment. Current evidence supports a critical role of excessive inflammation in ARDS, resulting in several cytokines, cytokine receptors, and proteins within their downstream signalling pathways being putative therapeutic targets. However, unsuccessful trials of anti-inflammatory drugs have thus far hindered progress in the field. In recent years, the prospects of precision medicine and therapeutic targeting of cytokines coevolving into effective treatments have gained notoriety. There is an optimistic and growing understanding of ARDS subphenotypes as well as advances in treatment strategies and clinical trial design. Furthermore, large trials of anti-cytokine drugs in patients with COVID-19 have provided an unprecedented amount of information that could pave the way for therapeutic breakthroughs. While current clinical and nonclinical ARDS research suggest relatively limited potential in monotherapy with anti-cytokine drugs, combination therapy has emerged as an appealing strategy and may provide new perspectives on finding safe and effective treatments. Accurate evaluation of these drugs, however, also relies on well-founded experimental research and the implementation of biomarker-guided stratification in future trials. In this review, we provide an overview of anti-cytokine therapy for acute lung injury and ARDS, highlighting the current preclinical and clinical evidence for targeting the main cytokines individually and the therapeutic prospects for combination therapy.

急性呼吸窘迫综合征(ARDS)是呼吸衰竭的一种异质性原因,发病迅速,死亡率高,而且没有有效的药物治疗。目前的证据支持过度炎症在ARDS中的关键作用,导致几种细胞因子、细胞因子受体及其下游信号通路中的蛋白质成为公认的治疗靶点。然而,迄今为止,抗炎药试验的失败阻碍了该领域的进展。近年来,精准医学和细胞因子靶向治疗共同转化为有效治疗的前景已经臭名昭著。人们对ARDS亚表型以及治疗策略和临床试验设计的进展有着乐观和不断增长的理解。此外,抗细胞因子药物在新冠肺炎患者中的大型试验提供了前所未有的信息,可能为治疗突破铺平道路。虽然目前的临床和非临床ARDS研究表明,抗细胞因子药物单药治疗的潜力相对有限,但联合治疗已成为一种有吸引力的策略,并可能为寻找安全有效的治疗方法提供新的视角。然而,对这些药物的准确评估也依赖于有充分依据的实验研究和在未来试验中实施生物标志物引导的分层。在这篇综述中,我们概述了抗细胞因子治疗急性肺损伤和ARDS的概况,强调了目前单独靶向主要细胞因子的临床前和临床证据,以及联合治疗的治疗前景。
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引用次数: 0
mTOR in programmed cell death and its therapeutic implications mTOR与程序性细胞死亡及其治疗意义
IF 13 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.06.002
Yawen Xie, Xianli Lei, Guoyu Zhao, Ran Guo, Na Cui

Mechanistic target of rapamycin (mTOR), a highly conserved serine/threonine kinase, is involved in cellular metabolism, protein synthesis, and cell death. Programmed cell death (PCD) assists in eliminating aging, damaged, or neoplastic cells, and is indispensable for sustaining normal growth, fighting pathogenic microorganisms, and maintaining body homeostasis. mTOR has crucial functions in the intricate signaling pathway network of multiple forms of PCD. mTOR can inhibit autophagy, which is part of PCD regulation. Cell survival is affected by mTOR through autophagy to control reactive oxygen species production and the degradation of pertinent proteins. Additionally, mTOR can regulate PCD in an autophagy-independent manner by affecting the expression levels of related genes and phosphorylating proteins. Therefore, mTOR acts through both autophagy-dependent and -independent pathways to regulate PCD. It is conceivable that mTOR exerts bidirectional regulation of PCD, such as ferroptosis, according to the complexity of signaling pathway networks, but the underlying mechanisms have not been fully explained. This review summarizes the recent advances in understanding mTOR-mediated regulatory mechanisms in PCD. Rigorous investigations into PCD-related signaling pathways have provided prospective therapeutic targets that may be clinically beneficial for treating various diseases.

雷帕霉素(mTOR)是一种高度保守的丝氨酸/苏氨酸激酶,其机制靶点参与细胞代谢、蛋白质合成和细胞死亡。程序性细胞死亡(PCD)有助于消除衰老、受损或肿瘤细胞,对于维持正常生长、对抗病原微生物和维持身体稳态是必不可少的。mTOR在多种形式PCD的复杂信号通路网络中具有关键功能。mTOR可以抑制自噬,这是PCD调节的一部分。mTOR通过自噬来控制活性氧的产生和相关蛋白质的降解,从而影响细胞的存活。此外,mTOR可以通过影响相关基因和磷酸化蛋白的表达水平,以不依赖自噬的方式调节PCD。因此,mTOR通过自噬依赖性和非依赖性途径调节PCD。根据信号通路网络的复杂性,可以想象mTOR对PCD发挥双向调节作用,如脱铁性贫血,但其潜在机制尚未得到充分解释。这篇综述综述了在理解mTOR介导的PCD调控机制方面的最新进展。对PCD相关信号通路的严格研究提供了可能对治疗各种疾病临床有益的前瞻性治疗靶点。
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引用次数: 0
Modulation of IL-33/ST2 signaling as a potential new therapeutic target for cardiovascular diseases 调节IL-33/ST2信号作为心血管疾病潜在的新治疗靶点
IF 13 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.06.003
Punniyakoti Veeraveedu Thanikachalam , Srinivasan Ramamurthy , Poojitha Mallapu , Sudhir Rama Varma , Jayaraj Narayanan , Mohammed AS Abourehab , Prashant Kesharwani

IL-33 belongs to the IL-1 family of cytokines, which function as inducers of Th2 cytokine production by binding with ST2L and IL-1RAcP. This, in turn, activates various signaling pathways, including the mitogen-activated protein kinase (MAPK), the inhibitor of Kappa-B kinase (IKK) pathway, and the phospholipase D-sphingosine kinase pathway. IL-33 has demonstrated protective effects against various cardiovascular diseases (CVDs) by inducing Th2 cytokines and promoting alternative activating M2 polarization. However, the soluble decoy form of ST2 (sST2) mitigates the biological effects of IL-33, exacerbating CVDs. Furthermore, IL-33 also plays a significant role in the development of asthma, arthritis, atopic dermatitis, and anaphylaxis through the activation of Th2 cells and mast cells. In this review, we aim to demonstrate the protective role of IL-33 against CVDs from 2005 to the present and explore the potential of serum soluble ST2 (sST2) as a diagnostic biomarker for CVDs. Therefore, IL-33 holds promise as a potential therapeutic target for the treatment of CVDs.

IL-33属于IL-1细胞因子家族,其通过与ST2L和IL-1RAcP结合而发挥Th2细胞因子产生的诱导剂的作用。这反过来激活了各种信号通路,包括丝裂原活化蛋白激酶(MAPK)、Kappa-B激酶抑制剂(IKK)通路和磷脂酶D-鞘氨醇激酶通路。IL-33通过诱导Th2细胞因子和促进选择性激活M2极化,对各种心血管疾病(CVD)具有保护作用。然而,ST2的可溶性诱饵形式(sST2)减轻了IL-33的生物学效应,加剧了CVD。此外,IL-33还通过激活Th2细胞和肥大细胞在哮喘、关节炎、特应性皮炎和过敏反应的发展中发挥重要作用。在这篇综述中,我们旨在证明从2005年到现在IL-33对心血管疾病的保护作用,并探索血清可溶性ST2(sST2)作为心血管疾病诊断生物标志物的潜力。因此,IL-33有望成为治疗心血管疾病的潜在治疗靶点。
{"title":"Modulation of IL-33/ST2 signaling as a potential new therapeutic target for cardiovascular diseases","authors":"Punniyakoti Veeraveedu Thanikachalam ,&nbsp;Srinivasan Ramamurthy ,&nbsp;Poojitha Mallapu ,&nbsp;Sudhir Rama Varma ,&nbsp;Jayaraj Narayanan ,&nbsp;Mohammed AS Abourehab ,&nbsp;Prashant Kesharwani","doi":"10.1016/j.cytogfr.2023.06.003","DOIUrl":"10.1016/j.cytogfr.2023.06.003","url":null,"abstract":"<div><p><span>IL-33 belongs to the IL-1 family of cytokines, which function as inducers of Th2 cytokine production<span> by binding with ST2L and IL-1RAcP. This, in turn, activates various signaling pathways, including the mitogen-activated protein kinase (MAPK), the inhibitor of Kappa-B kinase (IKK) pathway, and the phospholipase </span></span><span>D</span><span><span><span>-sphingosine kinase pathway. IL-33 has demonstrated protective effects against various cardiovascular diseases (CVDs) by inducing Th2 cytokines and promoting alternative activating M2 polarization. However, the soluble decoy form of ST2 (sST2) mitigates the biological effects of IL-33, exacerbating CVDs. Furthermore, IL-33 also plays a significant role in the development of asthma, arthritis, atopic dermatitis, and </span>anaphylaxis through the activation of Th2 cells and mast cells. In this review, we aim to demonstrate the protective role of IL-33 against CVDs from 2005 to the present and explore the potential of serum soluble ST2 (sST2) as a diagnostic biomarker for CVDs. Therefore, IL-33 holds promise as a potential therapeutic target for the </span>treatment of CVDs.</span></p></div>","PeriodicalId":11132,"journal":{"name":"Cytokine & Growth Factor Reviews","volume":"71 ","pages":"Pages 94-104"},"PeriodicalIF":13.0,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10024789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
Targeting the metabolism and immune system in pancreatic ductal adenocarcinoma: Insights and future directions 针对胰腺导管腺癌的代谢和免疫系统:见解和未来方向
IF 13 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-06-01 DOI: 10.1016/j.cytogfr.2023.06.006
Dhana Sekhar Reddy Bandi , Sujith Sarvesh , Batoul Farran , Ganji Purnachandra Nagaraju , Bassel F. El-Rayes

Pancreatic cancer, specifically pancreatic ductal adenocarcinoma (PDAC), presents a challenging landscape due to its complex nature and the highly immunosuppressive tumor microenvironment (TME). This immunosuppression severely limits the effectiveness of immune-based therapies. Studies have revealed the critical role of immunometabolism in shaping the TME and influencing PDAC progression. Genetic alterations, lysosomal dysfunction, gut microbiome dysbiosis, and altered metabolic pathways have been shown to modulate immunometabolism in PDAC. These metabolic alterations can significantly impact immune cell functions, including T-cells, myeloid-derived suppressor cells (MDSCs), and macrophages, evading anti-tumor immunity. Advances in immunotherapy offer promising avenues for overcoming immunosuppressive TME and enhancing patient outcomes. This review highlights the challenges and opportunities for future research in this evolving field. By exploring the connections between immunometabolism, genetic alterations, and the microbiome in PDAC, it is possible to tailor novel approaches capable of improving immunotherapy outcomes and addressing the limitations posed by immunosuppressive TME. Ultimately, these insights may pave the way for improved treatment options and better outcomes for PDAC patients.

胰腺癌症,特别是胰腺导管腺癌(PDAC),由于其复杂的性质和高度免疫抑制的肿瘤微环境(TME),呈现出具有挑战性的前景。这种免疫抑制严重限制了基于免疫的治疗的有效性。研究揭示了免疫代谢在TME形成和影响PDAC进展中的关键作用。遗传改变、溶酶体功能障碍、肠道微生物组失调和代谢途径的改变已被证明可以调节PDAC的免疫代谢。这些代谢变化可以显著影响免疫细胞功能,包括T细胞、骨髓源性抑制细胞(MDSCs)和巨噬细胞,从而逃避抗肿瘤免疫。免疫疗法的进展为克服免疫抑制性TME和提高患者预后提供了有希望的途径。这篇综述强调了这一不断发展的领域未来研究的挑战和机遇。通过探索PDAC中免疫代谢、基因改变和微生物组之间的联系,有可能定制能够改善免疫治疗结果并解决免疫抑制TME带来的局限性的新方法。最终,这些见解可能为改善PDAC患者的治疗选择和更好的结果铺平道路。
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引用次数: 1
Pathogenic mechanisms of glucocorticoid-induced osteoporosis 糖皮质激素诱发骨质疏松症的发病机制。
IF 13 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-04-01 DOI: 10.1016/j.cytogfr.2023.03.002
Meng Chen , Wenyu Fu , Huiyun Xu , Chuan-ju Liu

Glucocorticoid (GC) is one of the most prescribed medicines to treat various inflammatory and autoimmune diseases. However, high doses and long-term use of GCs lead to multiple adverse effects, particularly glucocorticoid-induced osteoporosis (GIO). Excessive GCs exert detrimental effects on bone cells, including osteoblasts, osteoclasts, and osteocytes, leading to impaired bone formation and resorption. The actions of exogenous GCs are considered to be strongly cell-type and dose dependent. GC excess inhibits the proliferation and differentiation of osteoblasts and enhances the apoptosis of osteoblasts and osteocytes, eventually contributing to reduced bone formation. Effects of GC excess on osteoclasts mainly include enhanced osteoclastogenesis, increased lifespan and number of mature osteoclasts, and diminished osteoclast apoptosis, which result in increased bone resorption. Furthermore, GCs have an impact on the secretion of bone cells, subsequently disturbing the process of osteoblastogenesis and osteoclastogenesis. This review provides timely update and summary of recent discoveries in the field of GIO, with a particular focus on the effects of exogenous GCs on bone cells and the crosstalk among them under GC excess.

糖皮质激素(GC)是治疗各种炎症和自身免疫性疾病的最常用药物之一。然而,高剂量和长期使用GC会导致多种不良反应,特别是糖皮质激素诱导的骨质疏松症(GIO)。过量的GC对骨细胞(包括成骨细胞、破骨细胞和骨细胞)产生有害影响,导致骨形成和吸收受损。外源GC的作用被认为是强烈的细胞类型和剂量依赖性的。GC过量抑制成骨细胞的增殖和分化,增强成骨细胞和骨细胞的凋亡,最终导致骨形成减少。GC过量对破骨细胞的影响主要包括破骨细胞生成增强、成熟破骨细胞寿命和数量增加以及破骨细胞凋亡减少,从而导致骨吸收增加。此外,GC对骨细胞的分泌有影响,从而干扰成骨细胞和破骨细胞的生成过程。这篇综述及时更新和总结了GIO领域的最新发现,特别关注外源GC对骨细胞的影响以及在GC过量的情况下它们之间的串扰。
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引用次数: 6
Role of cellular senescence in inflammatory lung diseases 细胞衰老在炎性肺病中的作用
IF 13 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-04-01 DOI: 10.1016/j.cytogfr.2023.02.001
Cong Xie , Mai Maititusun Ya Likun , Qing-li Luo , Jing-cheng Dong

Cellular senescence, a characteristic sign of aging, classically refers to permanent cell proliferation arrest and is a vital contributor to the pathogenesis of cancer and age-related illnesses. A lot of imperative scientific research has shown that senescent cell aggregation and the release of senescence-associated secretory phenotype (SASP) components can cause lung inflammatory diseases as well. In this study, the most recent scientific progress on cellular senescence and phenotypes was reviewed, including their impact on lung inflammation and the contributions of these findings to understanding the underlying mechanisms and clinical relevance of cell and developmental biology. Within a dozen pro-senescent stimuli, the irreparable DNA damage, oxidative stress, and telomere erosion are all crucial in the long-term accumulation of senescent cells, resulting in sustained inflammatory stress activation in the respiratory system. An emerging role for cellular senescence in inflammatory lung diseases was proposed in this review, followed by the identification of the main ambiguities, thus further understanding this event and the potential to control cellular senescence and pro-inflammatory response activation. In addition, novel therapeutic strategies for the modulation of cellular senescence that might help to attenuate inflammatory lung conditions and improve disease outcomes were also presented in this research.

细胞衰老是衰老的一个特征性标志,通常指的是永久性细胞增殖停滞,是癌症和年龄相关疾病发病机制的重要因素。大量必要的科学研究表明,衰老细胞聚集和衰老相关分泌表型(SASP)成分的释放也会导致肺部炎症性疾病。在这项研究中,回顾了细胞衰老和表型的最新科学进展,包括它们对肺部炎症的影响,以及这些发现对理解细胞和发育生物学的潜在机制和临床相关性的贡献。在十几种促衰老刺激中,无法修复的DNA损伤、氧化应激和端粒侵蚀都是衰老细胞长期积累的关键,导致呼吸系统持续的炎症应激激活。这篇综述提出了细胞衰老在炎症性肺病中的一个新作用,随后确定了主要的歧义,从而进一步了解了这一事件以及控制细胞衰老和促炎反应激活的潜力。此外,本研究还提出了调节细胞衰老的新治疗策略,这些策略可能有助于减轻炎症性肺部疾病并改善疾病结果。
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引用次数: 4
Immune evasion of neutralizing antibodies by SARS-CoV-2 Omicron SARS-CoV-2组粒对中和抗体的免疫逃避
IF 13 2区 医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Pub Date : 2023-04-01 DOI: 10.1016/j.cytogfr.2023.03.001
Lidong Wang , Michelle Møhlenberg , Pengfei Wang , Hao Zhou

Since its emergence at the end of 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused the infection of more than 600 million people worldwide and has significant damage to global medical, economic, and political structures. Currently, a highly mutated variant of concern, SARS-CoV-2 Omicron, has evolved into many different subvariants mainly including BA.1, BA.2, BA.3, BA.4/5, and the recently emerging BA.2.75.2, BA.2.76, BA.4.6, BA.4.7, BA.5.9, BF.7, BQ.1, BQ.1.1, XBB, XBB.1, etc. Mutations in the N-terminal domain (NTD) of the spike protein, such as A67V, G142D, and N212I, alter the antigenic structure of Omicron, while mutations in the spike receptor binding domain (RBD), such as R346K, Q493R, and N501Y, increase the affinity for angiotensin-converting enzyme 2 (ACE2). Both types of mutations greatly increase the capacity of Omicron to evade immunity from neutralizing antibodies, produced by natural infection and/or vaccination. In this review, we systematically assess the immune evasion capacity of SARS-CoV-2, with an emphasis on the neutralizing antibodies generated by different vaccination regimes. Understanding the host antibody response and the evasion strategies employed by SARS-CoV-2 variants will improve our capacity to combat newly emerging Omicron variants.

自2019年底出现以来,严重急性呼吸系统综合征冠状病毒2型已在全球造成6亿多人感染,并对全球医疗、经济和政治结构造成重大损害。目前,严重急性呼吸系统综合征冠状病毒2型奥密克戎的一种高度突变变体已进化成许多不同的亚变体,主要包括BA.1、BA.2、BA.3、BA.4/5和最近出现的BA.2.75.2、BA.2.76、BA.4.6、BA.4.7、BA.5.9、BF.7、BQ.1、BQ.1.1、XBB、XBB.1等。刺突蛋白N端结构域(NTD)的突变,如A67V、G142D和N212I,改变了奥密克龙的抗原结构,而刺突受体结合结构域(RBD)的突变,如R346K、Q493R和N501Y,增加了对血管紧张素转换酶2(ACE2)的亲和力。这两种类型的突变都大大增加了奥密克戎逃避自然感染和/或疫苗接种产生的中和抗体免疫的能力。在这篇综述中,我们系统地评估了严重急性呼吸系统综合征冠状病毒2型的免疫逃避能力,重点是不同疫苗接种制度产生的中和抗体。了解宿主抗体反应和严重急性呼吸系统综合征冠状病毒2型变异株采用的逃避策略将提高我们对抗新出现的奥密克戎变异株的能力。
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引用次数: 12
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