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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

Understanding the Skeletal Pathology of Type 1 and 2 Diabetes Mellitus

Volume 21, Issue 2, 2011, pp. 187-206
DOI: 10.1615/CritRevEukarGeneExpr.v21.i2.70
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ABSTRACT

Diabetes affects over 25 million people and is characterized by hyperglycemia resulting from a lack of insulin or reduced insulin sensitivity. A serious complication of diabetes is the increase in fracture risk observed in both type 1 and type 2 diabetic patients. This review focuses on some of the cellular and mechanistic causes of diabetes-induced fracture risk. Type 1 and type 2 diabetes most likely have unique and overlapping mechanisms of bone loss. While type 1 diabetes is associated with reduced bone mineral density, this is not usually seen in type 2 diabetes. Hyperglycemia, present in both type 1 and 2 diabetes, alters bone matrix proteins such as collagen I through nonenzymatic glycation, which can decrease bone toughness and increase fracture risk even in the absence of bone loss. Diabetes is also associated with increased inflammation and altered adipokine and calcitrophic hormone levels, which further contribute to bone pathophysiology. As medical advances significantly lengthen patient lifespan, exposure to diabetic conditions increases and correspondingly so do disease complications. Further research to identify molecular pathways in diabetes-associated bone pathology will provide the basis for therapeutic targets/directions to increase treatment options and improve patient health and well-being.

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