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Critical Reviews™ in Eukaryotic Gene Expression

Erscheint 6 Ausgaben pro Jahr

ISSN Druckformat: 1045-4403

ISSN Online: 2162-6502

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 1.6 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.2 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.3 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00058 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.33 SJR: 0.345 SNIP: 0.46 CiteScore™:: 2.5 H-Index: 67

Indexed in

The Control of Bone Growth by Parathyroid Hormone, Leptin, & Statins

Volumen 12, Ausgabe 1, 2002, 30 pages
DOI: 10.1615/CritRevEukaryotGeneExpr.v12.i1.20
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ABSTRAKT

There is a need for anabolic drugs that can stimulate bone growth, improve bone microarchitecture, accelerate fracture healing and thus restore bone strength to oteoporotics. The anabolic agents currently leading the way to the clinic are the parathroid hormone (PTH) and some of its adenylyl cyclase-stimulating fragments. Here we discuss what is known about the genes and their products that are stimulated by PTHR1 receptor signals and in four ways cause a large accumulation of bone-building osteoblasts. We will also discuss the currently controversial anabolic activity of the cholesterol-lowering statins and outline a possible mechanism by which they might stimulate BMP-2 expession and bone growth. Finally, we will present the growing evdence for the body’s “fat-o-stat” cytokine—leptin—indirectly restraining bone growth via a hypothalamic factor and at the same serving as a local autocrine/paracrine stimulator of osteoblast activity via IGF-I and an inhibitor of osteoclast generation by stimulating osteoblastic cells’ antiosteoclast OPG (osteoprotegerin) expression and reducing their proosteoclast RANKL expression.

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