Regulations of Retinal Inflammation: Focusing on Müller Glia
Frontiers in Cell and Developmental Biology, ISSN: 2296-634X, Vol: 10, Page: 898652
2022
- 24Citations
- 35Captures
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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
- Citations24
- Citation Indexes24
- 24
- Captures35
- Readers35
- 35
Review Description
Retinal inflammation underlies multiple prevalent retinal diseases. While microglia are one of the most studied cell types regarding retinal inflammation, growing evidence shows that Müller glia play critical roles in the regulation of retinal inflammation. Müller glia express various receptors for cytokines and release cytokines to regulate inflammation. Müller glia are part of the blood-retinal barrier and interact with microglia in the inflammatory responses. The unique metabolic features of Müller glia in the retina makes them vital for retinal homeostasis maintenance, regulating retinal inflammation by lipid metabolism, purine metabolism, iron metabolism, trophic factors, and antioxidants. miRNAs in Müller glia regulate inflammatory responses via different mechanisms and potentially regulate retinal regeneration. Novel therapies are explored targeting Müller glia for inflammatory retinal diseases treatment. Here we review new findings regarding the roles of Müller glia in retinal inflammation and discuss the related novel therapies for retinal diseases.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85132624183&origin=inward; http://dx.doi.org/10.3389/fcell.2022.898652; http://www.ncbi.nlm.nih.gov/pubmed/35573676; https://www.frontiersin.org/articles/10.3389/fcell.2022.898652/full; https://dx.doi.org/10.3389/fcell.2022.898652; https://www.frontiersin.org/journals/cell-and-developmental-biology/articles/10.3389/fcell.2022.898652/full
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