Regulatory effect of long-stranded non-coding RNA-CRNDE on neurodegeneration during retinal ischemia-reperfusion
Heliyon, ISSN: 2405-8440, Vol: 8, Issue: 10, Page: e10994
2022
- 3Citations
- 3Captures
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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.
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Metrics Details
- Citations3
- Citation Indexes3
- CrossRef2
- Captures3
- Readers3
Article Description
Ischemia/reperfusion (I/R) injury is a common pathological mechanism involved in many ocular diseases. I/R is characterized by microvascular dysfunction and neurodegeneration. However, the mechanisms of neurodegeneration induced by I/R remain largely unknown. This study showed that the expression of long non-coding RNA-CRNDE was significantly upregulated after retinal ischemia-reperfusion (RIR). LncRNA-CRNDE knockdown alleviated retinal neurodegeneration induced by RIR injury, as shown by decreased reactive gliosis and reduced retinal cells loss. Furthermore, lncRNA-CRNDE knockdown directly regulated Müller cell function and indirectly affected RGC function in vitro. In addition, lncRNA-CRNDE knockdown led to a significant reduction in the release of several cytokines after RIR. This study suggests that lncRNA-CRNDE is a promising therapeutic target for RIR.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S2405844022022824; http://dx.doi.org/10.1016/j.heliyon.2022.e10994; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85139728736&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/36276743; https://linkinghub.elsevier.com/retrieve/pii/S2405844022022824; https://dx.doi.org/10.1016/j.heliyon.2022.e10994
Elsevier BV
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