Disorders of complement regulation
Drug Discovery Today: Disease Models, ISSN: 1740-6757, Vol: 11, Page: 29-35
2014
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
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Review Description
Experiments in genetically engineered mice have elucidated the key role of the complement system in the pathogenesis of several renal disorders. This has led to the clinical evaluation of agents that inhibit complement activation in patients with complement-mediated kidney disease. Here we discuss the mouse models of lupus nephritis, C3 glomerulopathy and atypical hemolytic uremic syndrome, together with an inducible model of antiphospholipid syndrome. Evidence for and against therapeutic modulation of specific complement pathways in these disorders is presented.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S1740675714000322; http://dx.doi.org/10.1016/j.ddmod.2014.05.006; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84923054608&origin=inward; https://linkinghub.elsevier.com/retrieve/pii/S1740675714000322; https://dx.doi.org/10.1016/j.ddmod.2014.05.006
Elsevier BV
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