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Immunological mechanisms and therapeutic targets of fatty liver diseases

Cellular & Molecular Immunology 2021年第1期18卷 73-91页

作者： Hua Wang Wajahat Mehal laura e.nagy Yaron Rotman Department of Oncology the First Affiliated Hospital of Anhui Medical UniversityHefeiAnhuiChina InfIammation and Immune Mediated Diseases Laboratory of Anhui Province HefeiAnhuiChina West Haven VA Medical Center West Haven CT and Yale University School of MedicineNew HavenCTUSA Department of Inflammation and Immunity Cleveland ClinicClevelandOHUSA Department of Gastroenterology and Hepatology Center for Liver Disease ResearchCleveland ClinicClevelandOHUSA Department of Molecular Medicine Case Western Reserve UniversityClevelandOHUSA Liver and energy Metabolism Section Liver Diseases BranchNational Institute of Diabetes and Digestive and Kidney DiseasesNational Institutes of HealthBethesdaMDUSA

Alcoholic liver disease(ALD)and nonalcoholic fatty liver disease(NAFLD)are the two major types of chronic liver disease *** processes play key roles in the pathogeneses of fatty liver diseases,and continuous inflammation promotes the progression of alcoholic steatohepatitis(ASH)and nonalcoholic steatohepatitis(NASH).Although both ALD and NAFLD are closely related to inflammation,their respective developmental mechanisms differ to some ***,we review the roles of multiple immunological mechanisms and therapeutic targets related to the inflammation associated with fatty liver diseases and the differences in the progression of ASH and *** cell types in the liver,including macrophages,neutrophils,other immune cell types and hepatocytes,are involved in fatty liver disease *** addition,microRNAs(miRNAs),extracellular vesicles(eVs),and complement also contribute to the inflammatory process,as does intertissue crosstalk between the liver and the intestine,adipose tissue,and the nervous *** point out that inflammation also plays important roles in promoting liver repair and controlling bacterial *** the complex regulatory process of disrupted homeostasis during the development of fatty liver diseases may lead to the development of improved targeted therapeutic intervention strategies.

关键词： ALD NAFLD inflammation cytokine target immune

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Anti-inflammatory pathways and alcoholic liver disease: Role of an adiponectin/interleukin-10/heme oxygenase-1 pathway

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World Journal of Gastroenterology 2010年第11期16卷 1330-1336页

作者： Palash Mandal Michele T Pritchard laura e nagy Department of Pathobiology and Gastroenterology Cleveland ClinicLerner Research Institute/NE-40

The development of alcoholic liver disease (ALD) is a complex process involving both the parenchymal and non-parenchymal cells in the liver. enhanced inflammation in the liver during ethanol exposure is an important contributor to injury. Kupffer cells, the resident macrophages in liver, are particularly critical to the onset of ethanol-induced liver injury. Chronic ethanol exposure sensitizes Kupffer cells to activation by lipopolysaccharide via Toll-like receptor 4. This sensitization enhances production of inflammatory mediators, such as tumor necrosis factor-α and reactive oxygen species, that contribute to hepatocyte dysfunction, necrosis, apoptosis, and fibrosis. Impaired resolution of the inflammatory process probably also contributes to ALD. The resolution of inflammation is an active, highly coordinated response that can potentially be manipulated via therapeutic interventions to treat chronic inflammatory diseases. Recent studies have identif ied an adiponectin/interleukin-10/heme oxygenase-1 (HO-1) pathway that is profoundly effective in dampening the enhanced activation of innate immune responses in primary cultures of Kupffer cells, as well as in an in vivo mouse model of chronic ethanol feeding. Importantly, induction of HO-1 also reduces ethanol-induced hepatocellular apoptosis in this in vivo model. Based on these data, we hypothesize that the development of therapeutic agents to regulate HO-1 and its downstream targets could be useful in enhancing the resolution of inflammation during ALD and preventing progression of early stages of liver injury.

关键词： Liver disease Alcohol Macrophages Hemeoxygenase-1 Inflammation

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Synergistic interaction between C5a and NOD2 signaling in the regulation of chemokine expression in RAW 264.7 macrophages

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Advances in Bioscience and Biotechnology 2013年第8期4卷 30-37页

作者： Hui Tang Umme Amara Dora Tang Mark A. Barnes Christine McDonald laura e. nagy Departments of Pathobiology Cleveland Clinic Cleveland USA

The innate immune response is a complex process involving multiple pathogen-recognition receptors, including toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors. Complement is also a critical component of innate immunity. While complement is known to interact with TLR-mediated signals, the interactions between NOD-like receptors and complement are not well understood. Here we report a synergistic interaction between C5a and Nod2 signaling in RAW 264.7 marophages. Long-term treatment with muramyl dipeptide (MDP), a NOD2 ligand, enhanced C5a-mediated expression of chemokine mRNAs in RAW 264.7 cells. This response was dependent on NOD2 expression and was associated with a decrease in expression of C5L2, a receptor for C5a which acts as a negative modulator of C5a receptor (C5aR) activity. MDP amplified C5a-mediated phosphorylation of p38 MAPK. Treatment of RAW264.7 cells with an inhibitor of p38 attenuated the synergistic effects of C5aon MDP-primed cells on MIP-2, but not MCP-1, mRNA. In contrast, inhibition of AKT prevented C5a stimulation of MCP-1, but not MIP-2, mRNA, in MDP-primed cells. Taken together, these data demonstrated a synergistic interaction between C5a and NOD2 in the regulation of chemokine expression in macrophages, associated with a down-regulation of C5L2, a negative regulator of C5a receptor activity.

关键词： Anaphylatoxin C5L2 C5a Receptor Complement NOD2

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酒精性肝病的发病机制:实质细胞与非实质细胞间的相互作用

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胃肠病学 2011年第3期16卷 131-134页

作者： Jessica I COHeN laura e nagy 蒋晓玲巫协宁 Departments of Pathobiology Gastroenterology and HepatologyCleveland Clinic Department of Nutrition Case Western Reserve University

酒精性肝病(ALD)的发生是一个肝实质细胞与非实质细胞共同参与的复杂过程。乙醇对肝细胞的影响以细胞器应激为特征,肝细胞功能发生多种改变,并在乙醇暴露期间逐渐累积。这些改变包括氧化应激、线粒体功能障碍、甲基化能力降低、内质网... 详细信息

酒精性肝病(ALD)的发生是一个肝实质细胞与非实质细胞共同参与的复杂过程。乙醇对肝细胞的影响以细胞器应激为特征,肝细胞功能发生多种改变,并在乙醇暴露期间逐渐累积。这些改变包括氧化应激、线粒体功能障碍、甲基化能力降低、内质网应激、囊泡转运受损和蛋白酶体功能改变。肝细胞损伤部分归因于肝细胞对乙醇的代谢。乙醇暴露时肝窦内皮细胞结构完整性的改变和肝内炎症反应增强亦为肝损伤的重要成因。肝纤维化以肝星状细胞活化引起的细胞外基质蛋白沉积为特征。肝脏驻留型巨噬细胞Kupffer细胞对乙醇诱导肝损伤的发生尤为关键。长期乙醇暴露使Kupffer细胞对脂多糖通过Toll样受体4产生的激活作用敏感性增强。这一致敏作用使炎症介质如肿瘤坏死因子-α(TNF-α)和活性氧簇(ROS)产生增加,导致肝细胞功能异常、坏死凋亡以及细胞外基质蛋白产生,引起肝纤维化。本文对乙醇诱导肝损伤的进展过程中,肝实质细胞与非实质细胞间复杂的相互作用作一概述。

关键词：乙醇肝脏补体先天性免疫 Kupffer细胞

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Surgical treatment for liver cancer

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World Journal of Gastroenterology 2010年第8期16卷 927-933页

作者： Nicole C Tsim Adam e Frampton nagy A Habib Long R Jiao Department of Hepatopancreatobiliary Surgery Division of SurgeryHammersmith Hospital campusImperial College London

Primary liver cancer is amongst the commonest tumors worldwide,particularly in parts of the developing world,and is increasing in incidence. Over the past three decades,surgical hepatic resection has evolved from a high risk,resource intensive procedure with limited application,to a safe and commonly performed operation with a range of indications. This article reviews the approach to surgical resection for malignancies such as hepatocellular cancer,metastatic liver de-posits and neuroendocrine tumors. Survival data after resection is also reviewed,as well as indications for curative resection.

关键词： Liver cancer Surgical resection Indications Hepatocellular carcinoma Colorectal liver metastases Neuroendocrine tumors Non-colorectal non-neuroendo-crine

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Critiquing and Joining Intersections of Disaster,Conflict,and Peace Research

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International Journal of Disaster Risk Science 2020年第5期11卷 555-567页

作者： laura e.R.Peters Ilan Kelman College of earth.Ocean and Atmospheric SciencesOregon State UniversityCorvallis.OR 97331USA Institute for Risk and Disaster Reduction and Institute for Global HealthUniversity College LondonLondon WC1E 6BT.UK University of Agder.4630 Kristiansand Norway

Disaster research,conflict research,and peace research have rich and deep histories,yet they do not always fully intersect or learn from each other,even when they investigate if and how disasters lead to conflict or *** has tended to focus on investigating causal linkages between disaster(including those associated with climate change)and conflict,and disaster diplomacy emerged as a thread of explanatory research that investigates how and why disaster-related activities do and do not in fluence peace and ***,definitive conclusions on the disaster-conflict-peace nexus have evaded scientific consensus,in part due to conceptual,methodological,and interpretive differences among *** article highlights that this nexus would benefit from a more robust engagement with each field's foundational research that explores beyond binary and crude *** are concepts of destructive and constructive conflict;direct,structural,and cultural violence,and their relationships to vulnerability;negative and positive peace;and the ideals and realities of peacebuilding and conflict *** article demonstrates how integrated scholarship could open up and advance new lines of questioning,with implications for developing cohere nt research,policy,and *** article concludes by offering recommendations for how to better connect disaster,conflict,and peace research.

关键词： Climate change Conflict research Disaster diplomacy Disaster risk reduction Peace research

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Small heat shock protein B8:from cell functions to its involvement in diseases and potential therapeutic applications

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Neural Regeneration Research 2025年第10期20卷 2872-2886页

作者： Marta Chierichetti Riccardo Cristofani Valeria Crippa Veronica Ferrari Marta Cozzi elena Casarotto Paola Pramaggiore laura Cornaggia Guglielmo Patelli Ali Mohamed Margherita Piccolella Mariarita Galbiati Paola Rusmini Barbara Tedesco Angelo Poletti Laboratory of experimental Biology Dipartimento di Scienze Farmacologiche e Biomolecolari“Rodolfo Paoletti”(DiSFeB)Universitàdegli Studi di MilanoMilanItaly

Heat shock protein family B(small)member 8(HSPB8)is a 22 kDa ubiquitously expressed protein belonging to the family of small heat shock ***8 is involved in various cellular mechanisms mainly related to proteotoxic stress response and in other processes such as inflammation,cell division,and ***8 binds misfolded clients to prevent their aggregation by assisting protein refolding or degradation through chaperone-assisted selective *** line with this function,the pro-degradative activity of HSPB8 has been found protective in several neurodegenerative and neuromuscular diseases characterized by protein misfolding and *** cancer,HSPB8 has a dual role being capable of exerting either a pro-or an anti-tumoral activity depending on the pathways and factors expressed by the model of cancer under ***,HSPB8 exerts a protective function in different diseases by modulating the inflammatory response,which characterizes not only neurodegenerative diseases,but also other chronic or acute conditions affecting the nervous system,such as multiple sclerosis and intracerebellar *** note,HSPB8 modulation may represent a therapeutic approach in other neurological conditions that develop as a secondary consequence of other *** is the case of cognitive impairment related to diabetes mellitus,in which HSPB8 exerts a protective activity by assuring mitochondrial *** review aims to summarize the diverse and multiple functions of HSPB8 in different pathological conditions,focusing on the beneficial effects of its ***-based and alternative therapeutic approaches targeting HSPB8 and its regulated pathways will be discussed,emphasizing how new strategies for cell and tissue-specific delivery represent an avenue to advance in disease treatments.

关键词： aggregation autophagy cancer chaperone chaperone-assisted selective autophagy cognitive impairment HSPB8 neuroinflammation neuromuscular diseases therapy

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A modified intron of VRT2 drives glume and grain elongation in wheat

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Molecular Plant 2021年第9期14卷 1421-1423页

作者： laura e.Dixon Scott A.Boden Faculty of Biological Sciences University of LeedsLeeds LS29JTUK School of Agriculture Food and WineWaite Research InstituteUniversity of AdelaideGlen OsmondSA 5064Australia

Yield is a complex trait that is determined predominantly by the number,size,and weight of grain produced by a plant,which are all in fluenced by multiple genes and environ mental *** cereals,grain size is in flue need by envir on mental signals including nutrient availability and temperature,and by variation for genes that control the dimensions of a grain or the size of floral organs(e.g.,Heang and Sassa,2012;Brinton et al.,2017;Adamski et al.,2021;Liu et al.,2021;Xiao et al.,2021).Three recent studies have investigated subspecies of tetrapioid and hexapioid wheat that produce Ion ger grains,which form in florets that contain elongated floral structures(Adamski et al.,2021;Liu et al.,2021;Xiao et al.,2021);their findings provide new understanding of the genes controlling floret architecture,which could be used by breeders to enhance grain size and yield.

关键词： grain organs wheat

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WeAK TYPe INeQUALITY FOR THe MAXIMAL OPeRATOR OF WALSH-KACZMARZ-MARCINKIeWICZ MeANS

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Acta Mathematica Scientia 2016年第2期36卷 359-370页

作者： Ushangi GOGINAVA Karoly nagy Department of Mechanics and Mathematics Tbilisi State University Chavchavadze str. 1 Tbilisi 0128 Georgia Institute of Mathematics and Computer Sciences College of Nyiregyhdza SSstSi str. 31/B 4400 Nyiregyhdza Hungary

The main aim of this article is to prove that the maximal operator σ^k＊ of the Marcinkiewicz-Fejer means of the two-dimensional Fourier series with respect to Walsh- Kaczmarz system is bounded from the Hardy space H... 详细信息

关键词： Walsh-Kaczmarz system Marcinkiewicz-Fej^r means Maximal operator a.e.convergence weak type inequality

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Virtual drug design： Skpl-Skp2 inhibition targets cancer stem cells

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Asian Journal of Andrology 2013年第6期15卷 717-718页

作者： laura e Pascal Zhou Wang Department of Urology University of Pittsburgh School of Medicine Pittsburgh PA 15232 USA University of Pittsburgh Cancer Institute University of Pittsburgh School of Medicine Pittsburgh PA 15232 USA Department of Pharmacology and Chemical Biology University of Pittsburgh School of Medicine Pittsburgh PA 15232 USA

The dysregulation of pathways regulat-ing cellular function is a frequent hall-mark of cancer and the development of specific pathway inhibitors that alter tumor growth and progression are the focus of multiple recent studies. e3 ubiquitin ligases are a large group of diverse protein enzymes that specifically target proteins for dear- ance, and their importance to normal cel-lular function is illustrated in the many diseases associated with their loss of func- tion or inappropriate targeting. S-phase kinase-associated protein 2 （Skp2） is an F box protein that plays critical roles in cell-cycle progression, senescence, metabolism, and acts as an Skpl-Cullin-l-F box （SCF） ubiquitin ligase substrate recognition fac-tor. Overexpression of Skp2 is associated with poor prognosis and metastasis in many cancers and is a well validated drug target. In a recent report, Chart et al. have iden-tified an Skp2 inhibitor that selectively impairs Skp2 e3 ligase activity using an integrated virtual high-throughput drug screening and experimental validation approach. This Skp2 inhibitor restricts cancer stemness and potentiates sensitivity to chemotherapeutic agents in multiple ani-mal tumor models. These findings identify a new novel small molecule that targets the Skp2 and reduces tumor growth by attenu-ating aerobic glycolysis and inducing cel-lular senescence.

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