Evidence mapPaperPMID 37600520Full record

ReviewFrontiers in aging neuroscience2023

Melatonin: a promising neuroprotective agent for cerebral ischemia-reperfusion injury.

Majid Tozihi, Behrouz Shademan, Hadi Yousefi, Cigir Biray Avci, Alireza Nourazarian, Gholamreza Dehghan

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in aging neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  11. Melatonin Promotes B-Cell Maturation and Attenuates Post-Ischemic Immunodeficiency in a Murine Model of Transient Focal Cerebral Ischemia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
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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 at 4 institutions in 2 countries.

Majid TozihiDepartment of Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran.
Behrouz ShademanStem Cell Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Hadi YousefiDepartment of Basic Medical Sciences, Khoy University of Medical Sciences, Khoy, Iran.
Cigir Biray AvciDepartment of Medical Biology, Faculty of Medicine, EGE University, Izmir, Türkiye.
Alireza NourazarianDepartment of Basic Medical Sciences, Khoy University of Medical Sciences, Khoy, Iran.
Gholamreza DehghanDepartment of Biology, Faculty of Natural Sciences, University of Tabriz, Tabriz, Iran.
Islamic Azad University, Khoy Branch · IRUniversity of Tabriz · IREge University · TRTabriz University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebral ischemia-reperfusion (CIR) injury is initiated by the generation of reactive oxygen species (ROS), which leads to the oxidation of cellular proteins, DNA, and lipids as an initial event. The reperfusion process impairs critical cascades that support cell survival, including mitochondrial biogenesis and antioxidant enzyme activity. Failure to activate prosurvival signals may result in increased neuronal cell death and exacerbation of CIR damage. Melatonin, a hormone produced naturally in the body, has high concentrations in both the cerebrospinal fluid and the brain. However, melatonin production declines significantly with age, which may contribute to the development of age-related neurological disorders due to reduced levels. By activating various signaling pathways, melatonin can affect multiple aspects of human health due to its diverse range of activities. Therefore, understanding the underlying intracellular and molecular mechanisms is crucial before investigating the neuroprotective effects of melatonin in cerebral ischemia-reperfusion injury.

Indexed as

cerebral ischemia-reperfusion injuryischemic strokesmelatoninneuroprotective agentreactive oxygen species (ROS)

Identifiers

PMID37600520
PMCPMC10436333
OpenAlexW4385583976

What Socratic 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 Socratic graph.