Islet inflammation in type 2 diabetes
Seminars in Immunopathology, ISSN: 1863-2300, Vol: 41, Issue: 4, Page: 501-513
2019
- 148Citations
- 257Captures
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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
- Citations148
- Citation Indexes148
- 148
- CrossRef106
- Captures257
- Readers257
- 257
Review Description
Metabolic diseases including type 2 diabetes are associated with meta-inflammation. β-Cell failure is a major component of the pathogenesis of type 2 diabetes. It is now well established that increased numbers of innate immune cells, cytokines, and chemokines have detrimental effects on islets in these chronic conditions. Recently, evidence emerged which points to initially adaptive and restorative functions of inflammatory factors and immune cells in metabolism. In the following review, we provide an overview on the features of islet inflammation in diabetes and models of prediabetes. We separately emphasize what is known on islet inflammation in humans and focus on in vivo animal models and how they are used to elucidate mechanistic aspects of islet inflammation. Further, we discuss the recently emerging physiologic signaling role of cytokines during adaptation and normal function of islet cells.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85064443601&origin=inward; http://dx.doi.org/10.1007/s00281-019-00745-4; http://www.ncbi.nlm.nih.gov/pubmed/30989320; http://link.springer.com/10.1007/s00281-019-00745-4; https://dx.doi.org/10.1007/s00281-019-00745-4; https://link.springer.com/article/10.1007/s00281-019-00745-4
Springer Science and Business Media LLC
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