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  1. Article: Systemic sclerosis: a prototypic multisystem fibrotic disorder.

    Varga, John / Abraham, David

    The Journal of clinical investigation

    2007  Volume 117, Issue 3, Page(s) 557–567

    Abstract: A unique feature of systemic sclerosis (SSc) that distinguishes it from other fibrotic disorders is ... in this prototypic multisystemic fibrotic disease. ... that shed light on the cellular and molecular mechanisms underlying the fibrotic process in SSc and ...

    Abstract A unique feature of systemic sclerosis (SSc) that distinguishes it from other fibrotic disorders is that autoimmunity and vasculopathy characteristically precede fibrosis. Moreover, fibrosis in SSc is not restricted to a single organ, but rather affects many organs and accounts for much of the morbidity and mortality associated with this disease. Although immunomodulatory drugs have been used extensively in the treatment of SSc, no therapy to date has been able to reverse or slow the progression of tissue fibrosis or substantially modify the natural progression of the disease. In this Review, we highlight recent studies that shed light on the cellular and molecular mechanisms underlying the fibrotic process in SSc and that identify cellular processes and intra- and extracellular proteins as potential novel targets for therapy in this prototypic multisystemic fibrotic disease.
    MeSH term(s) Animals ; Autoimmunity ; Blood Vessels/pathology ; Disease Models, Animal ; Fibrosis ; Scleroderma, Systemic/etiology ; Scleroderma, Systemic/immunology ; Scleroderma, Systemic/pathology
    Language English
    Publishing date 2007-03
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI31139
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: Abnormalities in endothelial form of nitric oxide synthase is pathogenic in limited cutaneous systemic sclerosis.

    Jia, Xiu-Juan / Mu, Qi-Ri / Lei, Tie-Chi

    Journal of cosmetic dermatology

    2019  Volume 18, Issue 6, Page(s) 1938–1946

    Abstract: ... characterized by a prototypic multisystem fibrotic disorder.: Objective: This study aimed to further ... Background: Limited cutaneous systemic sclerosis is one subtype of systemic sclerosis which is ... investigate the pathological mechanism of limited cutaneous systemic sclerosis (lcSSc).: Methods ...

    Abstract Background: Limited cutaneous systemic sclerosis is one subtype of systemic sclerosis which is characterized by a prototypic multisystem fibrotic disorder.
    Objective: This study aimed to further investigate the pathological mechanism of limited cutaneous systemic sclerosis (lcSSc).
    Methods: The dataset GSE76807 generated from 10 lcSSc patients and five healthy controls was used. After the preprocessing of the original data, differentially expressed genes (DEGs) were identified and then performed functional analysis, protein-protein interaction (PPI) network and module analysis. Additionally, the transcription factors (TFs) and miRNAs which potentially regulating DEGs were identified and the co-regulatory network was constructed. Finally, DEGs targeted by current drugs were identified. Real-time quantitative PCR analyses of some DEGs in mice with lcSSc were performed.
    Results: Total 203 up-regulated and 189 down-regulated DEGs were obtained. The up-regulated genes were enriched in protein interactions at the synapses neuronal system, NCAM1 interactions, and CREB phosphorylation through the activation of CaMKII, while, cilium assembly, and endothelial form of nitric oxide synthase (eNOS) activation were enriched by down-regulated genes. SCRT2 and RABEP1 regulated by miR-218 were hub nodes in the network. DRD4 and GRIN2D were the main drug targets. RABEP1 and SSB were found lowly expressed in mice model with lcSSc.
    Conclusion: Endothelial form of NOS activation would be suppressed, and the process of neuronal migration and outgrowth would be activated to participant in the pathological mechanism of lcSSc.
    MeSH term(s) Animals ; Gene Expression Regulation ; Humans ; Mice ; Nitric Oxide Synthase Type III/genetics ; Scleroderma, Systemic/genetics ; Scleroderma, Systemic/pathology
    Chemical Substances Nitric Oxide Synthase Type III (EC 1.14.13.39)
    Language English
    Publishing date 2019-04-13
    Publishing country England
    Document type Journal Article
    ZDB-ID 2280551-5
    ISSN 1473-2165 ; 1473-2130
    ISSN (online) 1473-2165
    ISSN 1473-2130
    DOI 10.1111/jocd.12917
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6539: Show issues Location:
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