Evidence map›Paper›PMID 31467256›Full record

ArticleAging2019

MicroRNA-181a protects against pericyte apoptosis via directly targeting FOXO1: implication for ameliorated cognitive deficits in APP/PS1 mice.

Qingbin Wu, Xiaochen Yuan, Jing Bai, Ruiqin Han, Zhigang Li, Honggang Zhang, Ruijuan Xiu

Open access · greenAbstract read
In one paragraph

Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

27 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Chlorpyrifos and Chlorpyrifos-Oxon: A Widening Spectrum of Toxicity.International journal of molecular sciences · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
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  10. Review
  11. Review
  12. Article
  13. Article
  14. Effect of Cannabidiolic Acid,Current issues in molecular biology · 2022
    Article
  15. Review
  16. Review
  17. Suppression of Fli-1 protects against pericyte loss and cognitive deficits in Alzheimer's disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Article
  18. Review
  19. Article
  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

7 authors at 3 institutions in 1 country.

Qingbin WuKey Laboratory for Microcirculation, Ministry of Health, Institute of Microcirculation, Chinese Academy Medical Sciences and Pecking Union Medical College, Beijing, China.
Xiaochen YuanKey Laboratory for Microcirculation, Ministry of Health, Institute of Microcirculation, Chinese Academy Medical Sciences and Pecking Union Medical College, Beijing, China.
Jing BaiDepartment of Pharmacy, the Fourth Hospital of Hebei Medical University, Shijiazhuang, China.
Ruiqin HanInstitute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine Peking Union Medical College, Beijing, China.
Zhigang LiSchool of Acupuncture, Moxibustion and Tuina, Beijing University of Chinese Medicine, Beijing, China.
Honggang ZhangKey Laboratory for Microcirculation, Ministry of Health, Institute of Microcirculation, Chinese Academy Medical Sciences and Pecking Union Medical College, Beijing, China.
Ruijuan XiuKey Laboratory for Microcirculation, Ministry of Health, Institute of Microcirculation, Chinese Academy Medical Sciences and Pecking Union Medical College, Beijing, China.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNBeijing University of Chinese Medicine · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MicroRNAs (miRNAs) have emerged as critical regulators in the pathology of Alzheimer's disease (AD). MiR-181a is associated with hippocampal memory formation and aberrantly expressed in patients with mild cognitive impairment (MCI), however, little is known about its role and underlying mechanism involved in AD. Here, we report that miR-181a expression declines in APP/PS1 mice, synchronous with the increase in amyloid β (Aβ) level, which suggests a reverse correlation between miR-181a level and AD development. Additionally, lentiviral overexpression of miR-181a via intrahippocampal injection ameliorates cognitive deficits and amyloid plaque deposition in APP/PS1 mice, indicating a beneficial role of miR-181a against AD progression. Moreover, miR-181a decelerates pericyte loss and blood-brain barrier breakdown in APP/PS1 mice. Furthermore, miR-181a protects against Aβ accumulation-induced pericyte apoptosis

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsApoptosisCognitive DysfunctionForkhead Box Protein O1HippocampusMiceMice, TransgenicMicroRNAsPericytesPresenilin-1Amyloid beta-Protein PrecursorForkhead Box Protein O1Foxo1 protein, mouseMicroRNAsmirn181 microRNA, mousePresenilin-1Alzheimer’s diseaseapoptosisFOXO1MicroRNA-181apericyte

Identifiers

PMID31467256
PMCPMC6738434
OpenAlexW2971242994

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.