Evidence map›Paper›PMID 32460803›Full record

ArticleCell communication and signaling : CCS2020

Exogenous fibroblast growth factor 1 ameliorates diabetes-induced cognitive decline via coordinately regulating PI3K/AKT signaling and PERK signaling.

Yanqing Wu, Chengbiao Wu, Libing Ye, Beini Wang, Yuan Yuan, Yaqian Liu, Peipei Zheng, Jun Xiong, Yiyang Li, Ting Jiang and 2 more

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  7. Review
  8. Aging · 2023
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  9. Review
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  11. Review
  12. Article
  13. Frontiers in neuroscience · 2022
    Article
  14. Article
  15. 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

12 authors at 2 institutions in 1 country.

Yanqing WuThe Institute of Life Sciences, Engineering Laboratory of Zhejiang province for pharmaceutical development of growth factors, Biomedical Collaborative Innovation Center of Wenzhou, Wenzhou University, Wenzhou, 325035, China.
Chengbiao WuClinical Research Center, Affiate Xiangshang Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, China.
Libing YeMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Beini WangMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Yuan YuanMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Yaqian LiuMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Peipei ZhengMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Jun XiongMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Yiyang LiMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Ting JiangMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Xiaokun LiMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China.
Jian XiaoMolecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, 325035, Zhejiang, China. xfxj2000@126.com.ORCID 0000-0001-7374-6506
Wenzhou Medical University · CNWenzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetes induces central nervous system damage, leading to cognitive decline. Fibroblast growth factor 1 (FGF1) has dual function of neuroprotection and normalizing hyperglycemia. To date, the precise mechanisms and potential treating strategies of FGF1 for diabetes-induced cognitive decline (DICD) hasn't been fully elucidated.

methodsIn this study, db/db mice were used as DICD animal model. We found that diabetes remarkably suppressed FGF1 expression in hippocampus. Thus, exogenous FGF1 had been treated for db/db mice and SH-SY5Y cells.

resultsFGF1 significantly ameliorates DICD with better spatial learning and memory function. Moreover, FGF1 blocked diabetes-induced morphological structure change, neuronal apoptosis and Aβ

conclusionWe conclude that FGF1 exerts its neuroprotective role and normalizing hyperglycemia effect, consequently ameliorates DICD, implying FGF1 holds a great promise to develop a new treatment for DICD. Video abstract.

Indexed as

AnimalsCell LineCognitive DysfunctionDiabetes ComplicationsDiabetes MellituseIF-2 KinaseFibroblast Growth Factor 1HumansMaleMiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionEIF2AK3 protein, humaneIF-2 KinaseFibroblast Growth Factor 1Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktcAMP-response element binding protein (CREB)Diabetes-induced cognitive decline (DICD)Fibroblast growth factor 1 (FGF1)HippocampusNeuronal apoptosisProtein kinase RNA-like ER kinase (PERK)

Identifiers

PMID32460803
PMCPMC7251863
OpenAlexW3028672565

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.