Evidence map›Paper›PMID 33063244›Full record

ArticleNeurochemical research2020

Exogenous CGRP Regulates Apoptosis and Autophagy to Alleviate Traumatic Brain Injury Through Akt/mTOR Signalling Pathway.

Jun Tian, Lei Yang, Pengfei Wang, Lijun Yang, Zhenzeng Fan

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.2field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Headache After Stroke: An Update for the Clinician.Current neurology and neuroscience reports · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. A narrative review of autophagy in migraine.Frontiers in neuroscience · 2025
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Calcitonin gene-related peptide inhibits neuronal apoptosis in heatstroke rats via PKA/p-CREB pathway.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2024
    Article
  17. Review
  18. Article
  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

5 authors at 2 institutions in 1 country.

Jun TianDepartment of Neurosurgery, Hebei Medical University, Shijiazhuang, Hebei Province, China.
Lei YangDepartment of Epidemiology and Statistics, School of Public Health, Hebei Medical University, Hebei Key Laboratory of Environment and Human Health, Shijiazhuang, China.
Pengfei WangDepartment of Neurosurgery, Hebei General Hospital, Shijiazhuang, Hebei Province, China.
Lijun YangDepartment of Neurosurgery, Hebei Medical University, Shijiazhuang, Hebei Province, China. yanglijun1981@163.com.
Zhenzeng FanDepartment of Neurosurgery, Hebei Medical University, Shijiazhuang, Hebei Province, China. Fanzhenzeng@126.com.ORCID http://orcid.org/0000-0002-8772-8736
Hebei Medical University · CNHebei General Hospital · CN

Funding

Hebei Medical Science Research Project 20150631Natural Science Foundation of Hebei Province H2018206325
6 · The paper itself

Abstract

With millions of traumatic brain injury (TBI) patients every year, TBI is regarded as one of the leading causes of human death and disability. Calcitonin gene-related peptide (CGRP) has been domenstrated to be a potential therapeutic target for TBI. However, the detailed effect and underlying mechanism of CGRP on the injured brain after TBI has hardly been investigated. In this work, we established TBI models of mice and injected CGRP before and after modelling to study its effects on the brain lesion, neurological functions and behaviours, neuron apoptosis and autophagy after TBI. Impacts of introduced CGRP on the activation of Akt/mTOR signalling in the cortical tissues surrounding injured areas after TBI were also evaluated. It was found that CGRP was reduced after TBI, and gradually restored over time. CGRP administration significantly restored the brain lesion induced by TBI. The permeability of blood-brain barrier and brain edema was increased dramatically after TBI, which was ameliorated by exogenous CGRP. Moreover, several neurological behaviour tests were performed, showing that CGRP introduction also relieved the cognitive abilities of mice which were impaired after TBI. Enhancing apoptosis and autophagy of neurons in the cortical tissues of injury sites following TBI were also alleviated by CGRP administration. Besides, CGRP-treated brain cortical tissues showed increased activation of Akt/mTOR signalling after TBI. Therefore, the results suggest that exogenous CGRP plays a neuroprotective role in the injuryed brain after TBI, to relieve cell apoptosis and autophagy, at least partially through Akt/mTOR signalling pathway. This finding also provides more evidence for the treatment of TBI through introducing exogenous CGRP or its related drugs.

Indexed as

AnimalsApoptosisAutophagyBlood-Brain BarrierBrainBrain EdemaBrain Injuries, TraumaticCalcitonin Gene-Related PeptideHumansMaleMice, Inbred BALB CMorris Water Maze TestNeuronsNeuroprotective AgentsOpen Field TestProto-Oncogene Proteins c-aktCalcitonin Gene-Related PeptidemTOR protein, mouseNeuroprotective AgentsProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesCGRPCognitionNeuronsSignal transductionTBI

Identifiers

PMID33063244
OpenAlexW3093354364

What OpenQuestion holds

Textmetadata
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.