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Resolvin D1 Halts Remote Neuroinflammation and Improves Functional Recovery after Focal Brain Damage Via ALX/FPR2 Receptor-Regulated MicroRNAs

Overview of attention for article published in Molecular Neurobiology, January 2018
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • Good Attention Score compared to outputs of the same age (79th percentile)
  • High Attention Score compared to outputs of the same age and source (84th percentile)

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1 blog
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1 Facebook page

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Title
Resolvin D1 Halts Remote Neuroinflammation and Improves Functional Recovery after Focal Brain Damage Via ALX/FPR2 Receptor-Regulated MicroRNAs
Published in
Molecular Neurobiology, January 2018
DOI 10.1007/s12035-018-0889-z
Pubmed ID
Authors

Elisa Bisicchia, Valeria Sasso, Giuseppina Catanzaro, Alessandro Leuti, Zein Mersini Besharat, Martina Chiacchiarini, Marco Molinari, Elisabetta Ferretti, Maria Teresa Viscomi, Valerio Chiurchiù

Abstract

Remote damage is a secondary phenomenon that usually occurs after a primary brain damage in regions that are distant, yet functionally connected, and that is critical for determining the outcomes of several CNS pathologies, including traumatic brain and spinal cord injuries. The understanding of remote damage-associated mechanisms has been mostly achieved in several models of focal brain injury such as the hemicerebellectomy (HCb) experimental paradigm, which helped to identify the involvement of many key players, such as inflammation, oxidative stress, apoptosis and autophagy. Currently, few interventions have been shown to successfully limit the progression of secondary damage events and there is still an unmet need for new therapeutic options. Given the emergence of the novel concept of resolution of inflammation, mediated by the newly identified ω3-derived specialized pro-resolving lipid mediators, such as resolvins, we reported a reduced ability of HCb-injured animals to produce resolvin D1 (RvD1) and an increased expression of its target receptor ALX/FPR2 in remote brain regions. The in vivo administration of RvD1 promoted functional recovery and neuroprotection by reducing the activation of Iba-1+ microglia and GFAP+ astrocytes as well as by impairing inflammatory-induced neuronal cell death in remote regions. These effects were counteracted by intracerebroventricular neutralization of ALX/FPR2, whose activation by RvD1 also down-regulated miR-146b- and miR-219a-1-dependent inflammatory markers. In conclusion, we propose that innovative therapies based on RvD1-ALX/FPR2 axis could be exploited to curtail remote damage and enable neuroprotective effects after acute focal brain damage.

X Demographics

X Demographics

The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 57 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 57 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 9 16%
Student > Master 9 16%
Student > Ph. D. Student 7 12%
Student > Bachelor 6 11%
Professor 3 5%
Other 8 14%
Unknown 15 26%
Readers by discipline Count As %
Neuroscience 15 26%
Biochemistry, Genetics and Molecular Biology 11 19%
Medicine and Dentistry 6 11%
Agricultural and Biological Sciences 2 4%
Immunology and Microbiology 2 4%
Other 3 5%
Unknown 18 32%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 8. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 09 April 2019.
All research outputs
#4,157,894
of 23,576,969 outputs
Outputs from Molecular Neurobiology
#868
of 3,558 outputs
Outputs of similar age
#90,633
of 443,387 outputs
Outputs of similar age from Molecular Neurobiology
#17
of 104 outputs
Altmetric has tracked 23,576,969 research outputs across all sources so far. Compared to these this one has done well and is in the 82nd percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 3,558 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.3. This one has done well, scoring higher than 75% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 443,387 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 79% of its contemporaries.
We're also able to compare this research output to 104 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 84% of its contemporaries.