Evidence map›Paper›PMID 37529236›Full record

ReviewFrontiers in neuroscience2023

Calcitonin gene-related peptide: a potential protective agent in cerebral ischemia-reperfusion injury.

Jie Xiong, Zhiyong Wang, Junhui Bai, Keling Cheng, Qicai Liu, Jun Ni

Abstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Observational
  6. Review
  7. Review
  8. Review
  9. Headache After Stroke: An Update for the Clinician.Current neurology and neuroscience reports · 2025
    Review
  10. Review
  11. Article
  12. A narrative review of autophagy in migraine.Frontiers in neuroscience · 2025
    Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. E3 ubiquitin ligase MARCH1 reduces inflammation and pyroptosis in cerebral ischemia-reperfusion injury via PCSK9 downregulation.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
    Article
  19. Article
  20. A review of theFrontiers in pharmacology · 2024
    Review
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

6 authors.

Jie XiongDepartment of Rehabilitation, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.
Zhiyong WangDepartment of Rehabilitation, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.
Junhui BaiDepartment of Rehabilitation, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.
Keling ChengDepartment of Rehabilitation, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.
Qicai LiuDepartment of Reproductive Medicine Centre, The First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
Jun NiDepartment of Rehabilitation, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemic stroke is the most common type of cerebrovascular disease with high disability and mortality rates, which severely burdens patients, their families, and society. At present, thrombolytic therapy is mainly used for the treatment of ischemic strokes. Even though it can achieve a good effect, thrombolytic recanalization can cause reperfusion injury. Calcitonin gene-related peptide (CGRP) is a neuropeptide that plays a neuroprotective role in the process of ischemia-reperfusion injury. By combining with its specific receptors, CGRP can induce vasodilation of local cerebral ischemia by directly activating the cAMP-PKA pathway in vascular smooth muscle cells and by indirectly activating the NO-cGMP pathway in an endothelial cell-dependent manner,thus rapidly increasing ischemic local blood flow together with reperfusion. CGRP, as a key effector molecule of neurogenic inflammation, can reduce the activation of microglia, downregulates Th1 classical inflammation, and reduce the production of TNF-α, IL-2, and IFN-γ and the innate immune response of macrophages, leading to the reduction of inflammatory factors. CGRP can reduce the overexpression of the aquaporin-4 (AQP-4) protein and its mRNA in the cerebral ischemic junction, and play a role in reducing cerebral edema. CGRP can protect endothelial cells from angiotensin II by reducing the production of oxidants and protecting antioxidant defense. Furthermore, CGRP-upregulated eNOS can further induce VEGF expression, which then promotes the survival and angiogenesis of vascular endothelial cells. CGRP can also reduce apoptosis by promoting the expression of Bcl-2 and inhibiting the expression of caspase-3. These effects suggest that CGRP can reduce brain injury and repair damaged nerve function. In this review, we focused on the role of CGRP in cerebral ischemia-reperfusion injury.

Indexed as

apoptosisbraincalcitonin gene-related peptideischemia–reperfusion injurynerve damage repair

Identifiers

PMID37529236
PMCPMC10387546

What OpenQuestion holds

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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.