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共215条结果
  • 1.

    【2hr】Suppl 1: Mediators of Fibrosis

    包量

    机译 补充1：纤维化的介导者
    摘要：
  • 2.

    【2hr】Suppl 1: New Insights into the Mechanisms of Innate Immune Receptor Signalling in Fibrosis

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    机译 增刊1：对纤维化中天然免疫受体信号传导机制的新见解
    摘要：Recent advances in our understanding of innate immunity and inflammation have direct bearing on how we understand autoimmunity, and fibrosis, and how innate immune sensors might stimulate both of these key features of several fibrotic diseases. Toll-like receptors (TLRs) are the major receptors for recognizing pathogen associated molecular patterns present on bacterial cell walls, such as LPS, and nucleic acids (RNA and DNA). Several intracellular pathways mediate TLR effects and initiate various pro-inflammatory programs. Mechanisms for control of inflammation, matrix remodeling, and ultimately fibrosis are also activated. Transforming growth factor-beta (TGF-β), Interleukin-1 (IL-1), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-13 (IL-13), and interferon (IFNs) appear particularly important in regulating pro-fibrotic aspects of innate immune activation. These mechanisms appear important in fibrotic disease affecting multiple organ-systems, including lung, liver, kidney, and skin. These observations provide new paradigms for understanding the relationship between immunity/inflammation and fibrosis, however, the precise ligand and mechanism linking innate immune sensor(s) to fibrosis remain uncertain in most illnesses.
  • 3.

    【2hr】Suppl 1: The Role of the NLRP3 Inflammasome in Fibrosis

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    机译 补充1：NLRP3炎性小体在纤维化中的作用
    • 作者：Carol M Artlett
    • 刊名：The Open Rheumatology Journal
    • 2012年第-1期
    摘要：Fibrosis leads to the deposition of collagens in organs and tissues. The resulting pathology induces a loss of function in the organ it is manifested in and this loss of function modulates the morbidity and mortality in that individual. Indeed, approximately 45% of all deaths in the Western world can be attributed to fibrosis and there are no FDA approved drugs for the treatment of fibrosis. The recent discovery of the inflammasome has led to a plethora of studies investigating this inflammatory signaling pathway in a wide variety of pathogen associated diseases. Many studies have focused on the NLRP3 inflammasome and this inflammasome is activated by a wide variety of cellular alarm signals. Once activated, caspase-1 is cleaved, inducing the secretion of IL-1β and IL-18 that signal to aid in the clearance of invading organisms. However, as the knowledge of the inflammasome has expanded, it was found that it can directly control collagen synthesis, leading to the increased deposition of collagens in the tissues such as the lung, liver, heart, and skin. Mice lacking the inflammasome adaptor protein, ASC, failed to become fibrotic when exposed to bleomycin. Inhibition of caspase-1 activity in fibroblasts from patients with the fibrotic disease systemic sclerosis, decreased collagen synthesis and reduced α-smooth muscle actin expression in myofibroblasts. Taken together, these observations suggest that the inflammasome can drive the fibrotic response and paves the way for novel therapeutics to be identified.
  • 4.

    【2hr】Suppl 1: New Insights into the Role of Oxidative Stress in Scleroderma Fibrosis

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    机译 补充1：氧化应激在硬皮病纤维化中作用的新见解
    摘要：Systemic sclerosis (Scleroderma – SSc) is a connective tissue disorder of unknown aetiology characterized by extensive fibrosis of the skin and visceral organs, by vascular abnormalities and immunological manifestations.Recent evidence suggest that the cellular redox state may play a significant role in the progression of scleroderma fibrosis. Mechanisms involved include an autoamplification circuit linking ROS, Ras and ERK 1-2 which in turn amplifies and maintains the autocrine loop made up by cytokines, growth factors and their cognate receptors.This review summarizes the recent progress on the role of oxidative stress in the pathophysiology of scleroderma and disorders characterised by organ fibrosis
  • 5.

    【2hr】Suppl 1: New Insights into the Mechanism of Notch Signalling in Fibrosis

    包量

    机译 增刊1：Notch信号在纤维化机制中的新见解
    摘要：The Notch pathway is an evolutionary conserved signalling mechanism that regulates cellular fate and development in various types of cells. The full spectrum of Notch effects has been well studied over the last decade in the fields of development and embryogenesis. But only recently several studies emphasized the involvement of the Notch signalling pathway in fibrosis. This review summarizes the structure and activation of the Notch family members, and focuses on recent findings regarding the role of Notch in organ fibrogenesis, in humans and in animal models.
  • 6.

    【2hr】Suppl 1: Regulation of Matrix Remodeling by Peroxisome Proliferator-Activated Receptor-γ: A Novel Link Between Metabolism and Fibrogenesis

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    机译 Suppl 1：过氧化物酶体增殖物激活的受体-γ对基质重塑的调节：代谢与纤维化之间的新型联系
    摘要：The intractable process of fibrosis underlies the pathogenesis of systemic sclerosis (SSc) and other diseases, and in aggregate contributes to 45% of deaths worldwide. Because currently there is no effective anti-fibrotic therapy, a better understanding of the pathways and cellular differentiation programs underlying fibrosis are needed. Emerging evidence points to a fundamental role of the nuclear hormone receptor peroxisome proliferator activated receptor-γ (PPAR-γ) in modulating fibrogenesis. While PPAR-γ has long been known to be important in lipid metabolism and in glucose homeostasis, its role in regulating mesenchymal cell biology and its association with pathological fibrosis had not been appreciated until recently. This article highlights recent studies revealing a consistent association of fibrosis with aberrant PPAR-γ expression and activity in various forms of human fibrosis and in rodent models, and reviews studies linking genetic manipulation of the PPAR-γ pathway in rodents and fibrosis. We survey the broad range of anti-fibrotic activities associated with PPAR-γ and the underlying mechanisms. We also summarize the emerging data linking PPAR-γ dysfunction and pulmonary arterial hypertension (PAH), which together with fibrosis is responsible for the mortality in patients in SSc. Finally, we consider current and potential future strategies for targeting PPAR-γ activity or expression as a therapy for controlling fibrosis.
  • 7.

    【2hr】Suppl 1: Caveolin-1 Signaling in Lung Fibrosis

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    机译 补充1：肺纤维化中的Caveolin-1信号传导
    摘要：Caveolin-1 is a master regulator of several signaling cascades because it is able to bind to and thereby inhibit members of a variety of kinase families. While associated with caveolae and involved in their generation, caveolin-1 is also present at other sites. A variety of studies have suggested that caveolin-1 may be a useful therapeutic target in fibrotic diseases of the lung and other tissues because in these diseases a low level of caveolin-1 expression is associated with a high level of collagen expression and fibrosis. Reduced caveolin-1 expression is observed not only in the fibroblasts that secrete collagen, but also in epithelial cells and monocytes. This is intriguing because both epithelial cells and monocytes have been suggested to be precursors of fibroblasts. Likely downstream effects of loss of caveolin-1 in fibrosis include activation of TGF-β signaling and upregulation of CXCR4 in monocytes resulting in their enhanced migration into damaged tissue where its ligand CXCL12 is produced. Finally, it may be possible to target caveolin-1 in fibrotic diseases without the use of gene therapy. A caveolin-1 peptide (caveolin-1 scaffolding domain) has been identified that retains the function of the full-length molecule to inhibit kinases and that can be modified by addition of the Antennapedia internalization sequence to allow it to enter cells both in vitro and in vivo.
  • 8.

    【2hr】Suppl 1: Sphingolipid Regulation of Tissue Fibrosis

    包量

    机译 补充1：鞘脂对组织纤维化的调节
    摘要：Bioactive sphingolipids, such as sphingosine 1-phosphate (S1P), dihydrosphingosine 1-phosphate (dhS1P) and ceramide, regulate a diverse array of cellular processes. Many of these processes are important components of wound-healing responses to tissue injury, including cellular apoptosis, vascular leak, fibroblast migration, and TGF-β signaling. Since over-exuberant or aberrant wound-healing responses to repetitive injury have been implicated in the pathogenesis of tissue fibrosis, these signaling sphingolipids have the potential to influence the development and progression of fibrotic diseases. Here we review accumulating in vitro and in vivo data indicating that these lipid mediators can in fact influence fibrogenesis in numerous organ systems, including the lungs, skin, liver, heart, and eye. Targeting these lipids, their receptors, or the enzymes involved in their metabolism consequently now appears to hold great promise for the development of novel therapies for fibrotic diseases.
  • 9.

    【2hr】Suppl 1: Role of MicroRNAs in Fibrosis

    包量

    机译 补充1：MicroRNA在纤维化中的作用
    摘要：Fibrosis is the leading cause of organ dysfunction in diseases such as systemic sclerosis, liver cirrhosis, cardiac fibrosis, progressive kidney disease, and idiopathic pulmonary fibrosis. The hallmark of fibrosis is tissue remodeling with excess deposition of extracellular matrix components, predominantly collagens. Different cell types, cytokines, growth factors, and enzymes interact in complex pathogenic networks with myofibroblasts playing a pivotal role. MicroRNAs are small non-coding RNAs acting as negative regulators of gene expression at the post-transcriptional level. MicroRNAs have been associated with many basic cellular processes as well as with a wide spectrum of diseases, most notably cancer. This review provides a comprehensive overview of microRNAs regulating profibrotic pathways and extracellular matrix synthesis. The potential of miRNA for targeted therapeutic approaches in fibrotic disorders is also discussed.
  • 10.

    【2hr】Suppl 1: Insulin-Like Growth Factor Binding Proteins-3 and -5: Central Mediators of Fibrosis and Promising New Therapeutic Targets

    包量

    机译 补充1：胰岛素样生长因子结合蛋白3和-5：纤维化的中枢介体和有希望的新治疗靶点
    摘要：Fibrosis involves an orchestrated cascade of events including activation of fibroblasts, increased production and deposition of extracellular matrix components, and differentiation of fibroblasts into myofibroblasts. Epithelial-mesenchymal cross-talk plays an important role in this process, and current hypotheses of organ fibrosis liken it to an aberrant wound healing response in which epithelial-mesenchymal transition (EMT) and cellular senescence may also contribute to disease pathogenesis. The fibrotic response is associated with altered expression of growth factors and cytokines, including increased levels of transforming growth factor-β1 (TGF-β1) and the more recent observation that increased levels of several insulin-like growth factor binding proteins (IGFBPs) are associated with a number of fibrotic conditions. IGFBPs have been implicated in virtually every cell type and process associated with the fibrotic response, making the IGFBPs attractive targets for the development of novel anti-fibrotic therapies. In this review, the current state of knowledge regarding the classical IGFBP family in organ fibrosis will be summarized and the clinical implications considered.
  • 11.

    【2hr】Suppl 1: The Function of SPARC as a Mediator of Fibrosis

    包量

    机译 补充1：SPARC作为纤维化介质的功能
    摘要：Fibrosis is a common end-point of a number of different diseases such as hypertension, diabetes, liver cirrhosis, and those associated with chronic inflammation. Fibrosis is characterized by excessive deposition of extracellular matrix that interferes with normal tissue architecture and function. Increased expression of secreted protein acidic and rich in cysteine (SPARC) in fibrotic tissues has been reported in numerous studies. SPARC is a 43 kDa collagen-binding protein secreted from several different cell types into the extracellular matrix and has been shown to be anti-proliferative and counter-adhesive in vitro. SPARC is a matricellular protein; meaning SPARC is secreted into the extracellular space but does not serve a structural function. Instead, SPARC modulates interactions between cells and the surrounding extracellular matrix. In animal models of fibrotic disease and in human fibrotic tissues, elevated expression of SPARC has been reported in many tissues including heart, lungs, kidneys, liver, dermis, intestine, and eyes. In this review, we will summarize current studies that have examined the expression and functional importance of SPARC in various animal models of fibrosis and in human tissues. Although cellular mechanisms of SPARC in fibrosis remain to be fully elucidated, the studies summarized here provide impetus to further explore the efficacy of SPARC as a potential target for reducing fibrosis.
  • 12.

    【2hr】Suppl 1: The Role of TGF-β Receptors in Fibrosis

    包量

    机译 补充1：TGF-β受体在纤维化中的作用
    摘要：Recent advances in defining TGF-β signaling pathways have provided a new level of understanding of the role of this pleiotropic growth factor in the development of fibrosis. Here, we review selected topics related to the profibrotic role of TGF-β . We will discuss new insights into the mechanisms of ligand activation and the contribution of Erk1/2 MAPK, PI3K/FAK, and Endoglin/Smad1 signaling pathways to the process of fibrosis. There is growing evidence of the disease-specific alterations of the downstream components of the TGF-β signaling pathway that may be explored for the future therapeutic interventions.
  • 13.

    【2hr】Suppl 1: Getting Out of a Sticky Situation: Targeting the Myofibroblast in Scleroderma

    包量

    机译 补充1：摆脱困境：针对硬皮病中的肌成纤维细胞
    • 作者：Andrew Leask
    • 刊名：The Open Rheumatology Journal
    • 2012年第-1期
    摘要：There is no treatment for the fibrosis observed in scleroderma (systemic sclerosis, SSc). Although genome-wide expression profiling has suggested that differences in gene expression patters between non-lesional and lesional skin are minimal, phenotypically these areas of tissue are quite different. In fact, lesional areas of scleroderma patients can be distinguished by the presence of a differentiated form of fibroblast, termed the myofibroblast. This cell type expresses the highly contractile protein α-smooth muscle actin (α-SMA). Fibroblasts isolated from SSc lesions excessively synthesize, adhere to and contract extracellular matrix (ECM) and display activated adhesive signaling pathways. Strategies aimed at blocking myofibroblast differentiation, persistence and activity are therefore likely to be useful in alleviating the fibrosis in scleroderma.
  • 14.

    【2hr】Sicca Symptoms and their Association with Chronic Rhinosinusitis in a Community Sample

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    机译 社区样本中的Sicca症状及其与慢性鼻-鼻窦炎的关系
    摘要：Objective:To determine associations between sicca symptoms, chronic rhinosinusitis (CRS) symptoms and asthma in a community survey.
  • 15.

    【2hr】Delayed Positivization of Cerebral Angiography in Reversible CerebralVasoconstriction Syndrome (RCVS) Presenting with Recurrent SubarachnoidHaemorrhage

    包量

    机译 可逆性脑血管造影的延迟阳性。血管收缩综合征（RCVS）表现为蛛网膜下腔复发出血
    摘要：Benign angiopathy of the central nervous system is a clinical syndrome with evidence of reversible cerebral vasoconstriction (RCVS). Haemorrhagic stroke, either subarachnoid or intracerebral is an unusual presentation of RCVS. We describe a case of RCVS presenting with a subarachnoid haemorrhage (SAH), with rebleeding and onset of hydrocephalus during the first week, and, notably, delayed evidence of typical angiographic features after two negative prior exams. Normalization of the angiographic vasculitic-like lesions was documented at month +6. Repeated cerebral angiograms are mandatory to exclude this kind of disease, and the uncommon presentation of this case reinforces this concept.
  • 16.

    【2hr】Total Recovery from Monoclonal Gammopathy and Autoimmune Phenomena After Parathyroidectomy

    包量

    机译 甲状旁腺切除术后单克隆乳房病和自身免疫现象的完全恢复
    摘要：Based on the observation of a patient with a causal relationship between hyperparathyroidism and development of both autoimmune disease and paraproteinemia, we hypothesize a novel cause of autoimmunity triggered in the context of hyperparathyroidism.
  • 17.

    【2hr】Symptom-Modifying Effect of Chondroitin Sulfate in Knee Osteoarthritis: A Meta-Analysis of Randomized Placebo-Controlled Trials Performed with Structum®

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    机译 硫酸软骨素在膝骨关节炎中的症状改善作用：使用Structum®进行的随机安慰剂对照试验的荟萃分析
    摘要：Objective: To perform a meta-analysis of randomized double-blind placebo-controlled clinical trials to assess the efficacy of a specific chondroitin sulfate preparation (Structum®, Laboratoires Pierre Fabre, Castres; France) as a symptom-modifying drug in osteoarthritis (OA) of the knee.
  • 18.

    【2hr】Musculoskeletal Health Professional Use of Internet Resources for Personal and Patient Education: Results from an Online National Survey

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    机译 肌肉骨骼健康专业人员使用Internet资源进行个人和患者教育：在线全国调查的结果
    摘要：Objectives:To study the current practice of computer use in musculoskeletal health professionals for their education and that of their patients.
  • 19.

    【2hr】Combined Structural and Synovial Assessment for Improved Ultrasound Discrimination of Rheumatoid Osteoarthritic and Normal Joints: A Pilot Study

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    机译 结合结构和滑膜评估改善类风湿骨关节炎和正常关节的超声辨别力：一项初步研究
    摘要：Background:Current ultrasonographic scoring systems used to assess the degree of finger joint synovitis in rheumatoid arthritis (RA) are not designed for distinguishing healthy or osteoarthritis (OA) patients from those with RA in clinical settings.
  • 20.

    【2hr】Suppl 2: Signal Transduction Pathways in Chronic Inflammatory Rheumatic Diseases

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    机译 补充2：慢性炎性风湿病的信号转导途径
    • 作者：Andrew P Cope
    • 刊名：The Open Rheumatology Journal
    • 2012年第-1期
    摘要：
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