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Critical Reviews™ in Eukaryotic Gene Expression

Published 6 issues per year

ISSN Print: 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

Bone Modeling and Remodeling

Volume 19, Issue 3, 2009, pp. 219-233
DOI: 10.1615/CritRevEukarGeneExpr.v19.i3.40
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ABSTRACT

Bone modeling adapts structure to loading by changing bone size and shape and removes damage and so maintains bone strength. Remodeling is initiated by damage producing osteocyte apoptosis, which signals the location of damage via the osteocyte-canalicular system to endosteal lining cells that form the canopy of a bone remodeling compartment (BRC). Molecular signalling within the BRC between precursors, mature cells, cells of the immune system, and products of the resorbed matrix titrate the birth, work, and lifespan of this remodeling machinery to cither remove or form a net volume of bone.
Advancing age is associated with a reduction in the volume of bone resorbed by each basic multicellular unit (BMU), an even greater reduction in the volume of bone formed by each BMU producing a net negative BMU balance, and an increased remodeling rate in midlife in women and late in life in both sexes so that now many remodeling events erode bone while an age-related decline in periosteal apposition results in net bone loss and bone fragility. A better understanding of the mechanisms responsible for structural decay is likely to reveal new approaches to the prevention and reversal of bone fragility.

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