Evidence map›Paper›PMID 34572088›Full record

ArticleCells2021

Betulinic Acid Protects from Ischemia-Reperfusion Injury in the Mouse Retina.

Aytan Musayeva, Johanna C Unkrig, Mayagozel B Zhutdieva, Caroline Manicam, Yue Ruan, Panagiotis Laspas, Panagiotis Chronopoulos, Marie L Göbel, Norbert Pfeiffer, Christoph Brochhausen and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Glaucoma Animal Models beyond Chronic IOP Increase.International journal of molecular sciences · 2024
    Review
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  13. Article
  14. Article
  15. The Role of Hydrogen Sulfide Regulation of Autophagy in Liver Disorders.International journal of molecular sciences · 2022
    Review
  16. 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

15 authors at 2 institutions in 2 countries.

Aytan MusayevaDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Johanna C UnkrigDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Mayagozel B ZhutdievaDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Caroline ManicamDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Yue RuanDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Panagiotis LaspasDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Panagiotis ChronopoulosDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.ORCID 0000-0001-7524-2117
Marie L GöbelDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Norbert PfeifferDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.
Christoph BrochhausenInstitute of Pathology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.ORCID 0000-0002-6761-0247
Andreas DaiberDepartment of Cardiology 1, Laboratory of Molecular Cardiology, University Medical Center, Johannes Gutenberg University Mainz, Building 605, Langenbeckstrasse 1, 55131 Mainz, Germany.ORCID 0000-0002-2769-0094
Matthias OelzeDepartment of Cardiology 1, Laboratory of Molecular Cardiology, University Medical Center, Johannes Gutenberg University Mainz, Building 605, Langenbeckstrasse 1, 55131 Mainz, Germany.
Huige LiDepartment of Pharmacology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.ORCID 0000-0003-3458-7391
Ning XiaDepartment of Pharmacology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.ORCID 0000-0002-5553-1752
Adrian GerickeDepartment of Ophthalmology, University Medical Center, Johannes Gutenberg University Mainz, Langenbeckstrasse 1, 55131 Mainz, Germany.ORCID 0000-0002-3506-8465
Johannes Gutenberg University Mainz · DEMassachusetts Eye and Ear Infirmary · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ischemia/reperfusion (I/R) events are involved in the pathophysiology of numerous ocular diseases. The purpose of this study was to test the hypothesis that betulinic acid protects from I/R injury in the mouse retina. Ocular ischemia was induced in mice by increasing intraocular pressure (IOP) to 110 mm Hg for 45 min, while the fellow eye served as a control. One group of mice received betulinic acid (50 mg/kg/day p.o. once daily) and the other group received the vehicle solution only. Eight days after the I/R event, the animals were killed and the retinal wholemounts and optic nerve cross-sections were prepared and stained with cresyl blue or toluidine blue, respectively, to count cells in the ganglion cell layer (GCL) of the retina and axons in the optic nerve. Retinal arteriole responses were measured in isolated retinas by video microscopy. The levels of reactive oxygen species (ROS) were assessed in retinal cryosections and redox gene expression was determined in isolated retinas by quantitative PCR. I/R markedly reduced cell number in the GCL and axon number in the optic nerve of the vehicle-treated mice. In contrast, only a negligible reduction in cell and axon number was observed following I/R in the betulinic acid-treated mice. Endothelial function was markedly reduced and ROS levels were increased in retinal arterioles of vehicle-exposed eyes following I/R, whereas betulinic acid partially prevented vascular endothelial dysfunction and ROS formation. Moreover, betulinic acid boosted mRNA expression for the antioxidant enzymes SOD3 and HO-1 following I/R. Our data provide evidence that betulinic acid protects from I/R injury in the mouse retina. Improvement of vascular endothelial function and the reduction in ROS levels appear to contribute to the neuroprotective effect.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalBetulinic AcidMaleMiceMice, Inbred C57BLPentacyclic TriterpenesProtective AgentsReactive Oxygen SpeciesReperfusion InjuryRetinaAnti-Inflammatory Agents, Non-SteroidalBetulinic AcidPentacyclic TriterpenesProtective AgentsReactive Oxygen Speciesarteriolesbetulinic acidischemia-reperfusion injuryreactive oxygen speciesretina

Identifiers

PMID34572088
PMCPMC8469383
OpenAlexW3201168637

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.