Evidence map›Paper›PMID 34118791›Full record

ArticleAging2021

Melatonin protects against focal cerebral ischemia-reperfusion injury in diabetic mice by ameliorating mitochondrial impairments: involvement of the Akt-SIRT3-SOD2 signaling pathway.

Lian Liu, Quan Cao, Wenwei Gao, Bingyu Li, Zhongyuan Xia, Bo Zhao

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
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  9. Review
  10. Melatonin as a shield against skeletal muscle damage: A study on ischemia-reperfusion injury.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2025
    Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Vascular Aging in Ischemic Stroke.Journal of the American Heart Association · 2024
    Review
  18. Review
  19. Role of NADCellular and molecular neurobiology · 2023
    Review
  20. 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 at 2 institutions in 1 country.

Lian LiuDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Quan CaoDepartment of Ultrasound Imaging, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Wenwei GaoCritical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Bingyu LiDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Zhongyuan XiaDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Bo ZhaoDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic patients are more vulnerable to cerebral ischemia-reperfusion (CIR) injury and have a worse prognosis and higher mortality after ischemic stroke than non-diabetic counterparts. Melatonin can exert neuroprotective effects against CIR injury in nondiabetic animal models. However, its effects on diabetic CIR injury and the underlying mechanisms remain unclarified. Herein, we found that melatonin administration improved neurological deficit, cerebral infarct volume, brain edema, and cell viability, reduced mitochondrial swelling, reactive oxygen species generation, and cytoplasmic cytochrome C release, and increased mitochondrial antioxidant enzymes activities, adenosine triphosphate production, and mitochondrial membrane potential in both streptozotocin-induced diabetic mice and high glucose-treated HT22 cells. Importantly, melatonin also activated protein kinase B (Akt) and sirtuin 3 (SIRT3)/superoxide dismutase 2 (SOD2) signaling and upregulated mitochondrial biogenesis-related transcription factors. However, these effects were largely attenuated by LY294002 (a specific Akt signaling blocker) administration. Additionally, 3-TYP (a selective SIRT3 inhibitor) and SIRT3 siRNA inhibited the above protective effects of melatonin as well as the upregulation of SIRT3 and the decrease of SOD2 acetylation but did not affect the p-Akt/Akt ratio. Overall, we demonstrate that melatonin can alleviate CIR injury in diabetic mice by activating Akt-SIRT3-SOD2 signaling and subsequently improving mitochondrial damage.

Indexed as

AnimalsApoptosisBrain EdemaBrain IschemiaCell LineCell SurvivalChromonesDiabetes Mellitus, ExperimentalGlucoseMaleMelatoninMiceMice, Inbred C57BLMitochondriaMorpholinesNeuroprotective Agents2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesGlucoseMelatoninMorpholinesNeuroprotective AgentsProto-Oncogene Proteins c-aktSirt3 protein, mouseSirtuin 3Superoxide DismutaseSuperoxide Dismutase 2diabetesischemic strokemelatoninmitochondriatherapy

Identifiers

PMID34118791
PMCPMC8266371
OpenAlexW3168948487

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.