Evidence map›Paper›PMID 25806530›Full record

ArticlePloS one2015

Icariin induces synoviolin expression through NFE2L1 to protect neurons from ER stress-induced apoptosis.

Fei Li, Beixue Gao, Hongxin Dong, Jingshan Shi, Deyu Fang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
6.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. The Natural Occurring Compounds Targeting Endoplasmic Reticulum Stress.Evidence-based complementary and alternative medicine : eCAM · 2016
    Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 2 countries.

Fei LiDepartment of Pharmacology and the Key Laboratory of Basic Pharmacology of Guizhou Province, Zunyi Medical College, Zunyi, China; Department of Psychiatry and Behavioral Sciences, Northwestern University Feinberg School of Medicine, 303 E. Chicago Ave, Chicago, IL, 60611, United States of America.
Beixue GaoDepartment of Pathology, Northwestern University Feinberg School of Medicine, 303 E. Chicago Ave, Chicago, IL, 60611, United States of America.
Hongxin DongDepartment of Psychiatry and Behavioral Sciences, Northwestern University Feinberg School of Medicine, 303 E. Chicago Ave, Chicago, IL, 60611, United States of America.
Jingshan ShiDepartment of Pharmacology and the Key Laboratory of Basic Pharmacology of Guizhou Province, Zunyi Medical College, Zunyi, China.
Deyu FangDepartment of Pathology, Northwestern University Feinberg School of Medicine, 303 E. Chicago Ave, Chicago, IL, 60611, United States of America.
Northwestern University · USZunyi Medical University · CN

Funding

The roles of Sirt1, a deacetylase, in immune tolerance and autoimmunityR01AI079056 · NIAID · UNIVERSITY OF MISSOURI-COLUMBIA · PI FANG, DEYU · 2008 to 2017
$3.3M
Simultaneous Targeting of IRE1a in B Cells and Macrophages for Lupus TherapyR01AR066634 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI FANG, DEYU, ZHANG, KEZHONG · 2014 to 2018
$1.7M
The roles of Synoviolin in immune tolerance and autoimmunityR01AI108634 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI FANG, DEYU · 2014 to 2017
$1.5M
The roles of Sirt1, a deacetylase, in immune tolerance and autoimmunityR56AI079056 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI FANG, DEYU · 2012 to 2012
$386k
NIAID NIH HHS R01 AI079056NIAID NIH HHS R01AI079056NIAID NIH HHS R01 AI108634NIAID NIH HHS R01AI108634NIAMS NIH HHS R01 AR066634NIAMS NIH HHS R01AR066634
6 · The paper itself

Abstract

By suppressing neuronal apoptosis, Icariin is a potential therapeutic drug for neuronal degenerative diseases. The molecular mechanisms of Icariin anti-apoptotic functions are still largely unclear. In this report, we found that Icariin induces the expression of Synoviolin, an endoplasmic reticulum (ER)-anchoring E3 ubiquitin ligase that functions as a suppressor of ER stress-induced apoptosis. The nuclear factor erythroid 2-related factor 1 (NFE2L1) is responsible for Icariin-mediated Synoviolin gene expression. Mutation of the NFE2L1-binding sites in a distal region of the Synoviolin promoter abolished Icariin-induced Synoviolin promoter activity, and knockdown of NFE2L1 expression prevented Icariin-stimulated Synoviolin expression. More importantly, Icariin protected ER stress-induced apoptosis of PC12 cells in a Synoviolin-dependent manner. Therefore, our study reveals Icariin-induced Synoviolin expression through NFE2L1 as a previously unappreciated molecular mechanism underlying the neuronal protective function of Icariin.

Indexed as

AnimalsApoptosisEndoplasmic Reticulum StressFlavonoidsNeuronsNeuroprotective AgentsNF-E2-Related Factor 1PC12 CellsPromoter Regions, GeneticRatsUbiquitin-Protein LigasesFlavonoidsicariinNeuroprotective AgentsNF-E2-Related Factor 1Syvn1 protein, ratUbiquitin-Protein Ligases

Identifiers

PMID25806530
PMCPMC4373914
OpenAlexW1983392900

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.