ArticleInternational journal of ophthalmology2025
Ghrelin alleviates high glucose-induced retinal microvascular endothelial cell injury by activating Nrf2/HO-1 pathway to inhibit ferroptosis.
Article in International journal of ophthalmology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- Acteoside alleviates high glucose-induced ROS accumulation and ferroptosis in ARPE-19 cells by activating the NRF2 signaling pathway.Molecular biology reports · 2026Article
- A novel mechanism of chlorogenic acid against type 2 diabetes-induced diabetic retinopathy: suppressing ferroptosis via NRF2/xCT/GPX4 and STAT3 signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Desferrioxamine attenuating high glucose-induced ferroptosis and inflammatory responses in Müller glial cellsInternational journal of ophthalmology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the protective role of ghrelin against diabetic retinopathy (DR), focusing on its anti-ferroptotic mechanism in high glucose-induced retinal endothelial injury.
methodsFirst, small interfering RNA (siRNA)-mediated interference was conducted to knockdown nuclear factor erythroid 2-related factor 2 (Nrf2). Using reverse transcription-polymerase chain reaction (RT-PCR), the expression level of Nrf2 was determined from human retinal microvascular endothelial cells (HRMECs) transfected with either si-NC or si-Nrf2. After that, cells were treated with 10 nmol/L ghrelin and then cultured in a high glucose (30 mmol/L) environment. EdU assay was utilized to assess cell proliferation, while transmission electron microscopy was employed to observe mitochondrial morphology. Flow cytometry was used to measure the level of intracellular reactive oxygen species (ROS), and biochemical assays were conducted to detect malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), and ferrous iron (Fe
resultsUnder a high glucose environment, ghrelin could significantly promote the proliferation of HRMECs and mitochondrial status, remarkably decrease the levels of intracellular ROS and MDA, and up-regulate the level of GSH and SOD. Besides, ghrelin greatly reduced Fe
conclusionGhrelin attenuates high glucose-induced injury of retinal endothelial cells
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.