Cilia Action in Islets: Lessons From Mouse Models
Frontiers in Endocrinology, ISSN: 1664-2392, Vol: 13, Page: 922983
2022
- 5Citations
- 57Usage
- 11Captures
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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
- Citations5
- Citation Indexes5
- Usage57
- Downloads50
- Abstract Views7
- Captures11
- Readers11
- 11
Review Description
Primary cilia as a signaling organelle have garnered recent attention as a regulator of pancreatic islet function. These rod-like sensors exist on all major islet endocrine cell types and transduce a variety of external cues, while dysregulation of cilia function contributes to the development of diabetes. The complex role of islet primary cilia has been examined using genetic deletion targeting various components of cilia. In this review, we summarize experimental models for the study of islet cilia and current understanding of mechanisms of cilia regulation of islet hormone secretion. Consensus from these studies shows that pancreatic cilia perturbation can cause both endocrine and exocrine defects that are relevant to human disease. We discuss future research directions that would further elucidate cilia action in distinct groups of islet cells, including paracrine and juxtacrine regulation, GPCR signaling, and endocrine-exocrine crosstalk.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85133867497&origin=inward; http://dx.doi.org/10.3389/fendo.2022.922983; http://www.ncbi.nlm.nih.gov/pubmed/35813631; https://www.frontiersin.org/articles/10.3389/fendo.2022.922983/full; https://digitalcommons.wustl.edu/oa_4/131; https://digitalcommons.wustl.edu/cgi/viewcontent.cgi?article=1124&context=oa_4; https://dx.doi.org/10.3389/fendo.2022.922983; https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2022.922983/full
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