ArticleEye and vision (London, England)2022
The ghrelin-GHSR-1a pathway inhibits high glucose-induced retinal angiogenesis in vitro by alleviating endoplasmic reticulum stress.
Article in Eye and vision (London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 7 citations in OpenAlex.
- LEF1 influences diabetic retinopathy and retinal pigment epithelial cell ferroptosisWorld journal of diabetes · 2025Article
- Ghrelin alleviates high glucose-induced retinal microvascular endothelial cell injury by activating Nrf2/HO-1 pathway to inhibit ferroptosis.International journal of ophthalmology · 2025Article
- Hhatl Reduces Apoptosis of Müller Cells in Diabetic Retinopathy by Relieving Endoplasmic Reticulum Stress.International journal of endocrinology · 2025Article
- Changes in Circulating Acylated Ghrelin and Neutrophil Elastase in Diabetic Retinopathy.Medicina (Kaunas, Lithuania) · 2024Article
- Ghrelin inhibits autophagy mediated by AKT/mTOR pathway to ameliorate retinal angiogenesis induced by high glucose stress.International journal of ophthalmology · 2024Article
- Cortistatin deficiency reveals a dysfunctional brain endothelium with impaired gene pathways, exacerbated immune activation, and disrupted barrier integrity.Journal of neuroinflammation · 2023Article
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5 authors at 1 institution in 1 country.
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Abstract
backgroundTo investigate the effect of ghrelin, a brain-gut peptide hormone, on high glucose-induced retinal angiogenesis in vitro and explore its association with endoplasmic reticulum (ER) stress.
methodsHuman retinal microvascular endothelial cells (HRMECs) were first divided into control and high-glucose groups, and the mRNA and protein expression levels of the receptor for ghrelin [growth hormone secretin receptor 1a, (GHSR-1a)] in cells were determined. HRMECs were then treated with high glucose alone or in combination with ghrelin or siGHSR-1a, and cell viability, migration, tube formation and the expression of the ER stress-related proteins PERK, ATF4 and CHOP were detected. Finally, to clarify whether the effects of ghrelin are related to ER stress, tunicamycin, an inducer of ER stress, was used to treat HRMECs, and cell viability, cell migration, and tube formation were evaluated.
resultsGHSR-1a expression in HRMECs at both the mRNA and protein levels was inhibited by high-glucose treatment. Under high-glucose conditions, ghrelin promoted cell viability and inhibited migration and tube formation, which were blocked by siGHSR-1a treatment. Ghrelin inhibited the increases in the protein levels of p-PERK, ATF4 and CHOP induced by high-glucose treatment, and combination treatment with siGHSR-1a reversed this effect of ghrelin. When tunicamycin was added, the effects of ghrelin on cell viability, migration and tube formation were all weakened.
conclusionsThis study experimentally revealed that ghrelin can inhibit high glucose-induced retinal angiogenesis in vitro through GHSR-1a, and alleviation of ER stress may be one of the mechanisms underlying this effect.
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