Neuroimmune system-mediated renal protection mechanisms
Clinical and Experimental Nephrology, ISSN: 1437-7799, Vol: 25, Issue: 9, Page: 915-924
2021
- 9Citations
- 19Captures
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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
- Citations9
- Citation Indexes9
- CrossRef1
- Captures19
- Readers19
- 19
Review Description
The autonomic nervous system plays an important role in maintaining homeostasis in organisms. Recent studies have shown that it also controls inflammation by directly altering the function of the immune system. The cholinergic anti-inflammatory pathway (CAP) is one of the neural circuits operating through the vagus nerve. Acetylcholine released from the terminal of the vagus nerve, which is a parasympathetic nerve, acts on the α7 nicotinic acetylcholine receptor of macrophages and reduces inflammation in the body. Previous animal studies demonstrated that vagus nerve stimulation reduced renal ischemia–reperfusion injury. Furthermore, restraint stress and pulsed ultrasound had similar protective effects against kidney injury, which were mainly thought to be mediated by the CAP. Using optogenetics, which can stimulate specific nerves, it was also revealed that activation of the CAP by restraint stress was mediated by C1 neurons in the medulla oblongata. Nevertheless, there still remain many unclear points regarding the role of the nervous and immune systems in controlling renal diseases, and further research is needed.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85105007968&origin=inward; http://dx.doi.org/10.1007/s10157-021-02062-3; http://www.ncbi.nlm.nih.gov/pubmed/33877485; https://link.springer.com/10.1007/s10157-021-02062-3; https://dx.doi.org/10.1007/s10157-021-02062-3; https://link.springer.com/article/10.1007/s10157-021-02062-3
Springer Science and Business Media LLC
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