ArticleJournal of diabetes research2022
Ghrelin Mitigates High-Glucose-Induced Oxidative Damage and Apoptosis in Lens Epithelial Cells.
Article in Journal of diabetes research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- PANK4 Regulates YAP to Modulate the Glycolytic Pathway in LEC for Driving LECs-EMT in Early Diabetic Cataract Pathogenesis.Investigative ophthalmology & visual science · 2026Article
- SMP30 May protect human lens epithelial cells against high glucose-induced oxidative damage by regulating the Keap1/Nrf2/NQO1 pathway.Scientific reports · 2025Article
- MicroRNA-204-5p Attenuates Oxidative Stress, Apoptosis and Inflammation by Targeting TXNIP in Diabetic Cataract.Biochemical genetics · 2025Article
- Icariin interacts with IGFBP3 to alleviate diabetic cataract through PI3K/AKT signaling pathway.iScience · 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
- Ghrelin in Focus: Dissecting Its Critical Roles in Gastrointestinal Pathologies and Therapies.Current issues in molecular biology · 2024Review
- The role of gut microorganisms and metabolites in intracerebral hemorrhagic stroke: a comprehensive review.Frontiers in neuroscience · 2024Review
- Emerging Relevance of Ghrelin in Programmed Cell Death and Its Application in Diseases.International journal of molecular sciences · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress induced by high glucose (HG) plays an important role in the mechanism of diabetic cataract. Evidence has shown that effects from oxidative stress induced damage of lens or human lens epithelial (HLE) cells. Antioxidant supplementation is a plausible strategy to avoid oxidative stress and maintain the function of lens. Ghrelin have been used in treatment of many diseases. In this study, we found that ghrelin attenuated HG-induced loss of cell viability, reduced oxidative damage, and cell apoptosis in HLE cells. Ghrelin inhibited apoptosis through the downregulation of Bax and the upregulation of Bcl-2. Our results suggest that ghrelin could be considered as a promising therapeutic intervention for diabetic cataract. We also observed rat lens transparent in cultured media and examined lens histopathological changes. The results showed that ghrelin could inhibit the histopathological injury of lenses and ultrastructural changes induced by HG. In conclusion, ghrelin may play a role in the treatment of ocular diseases involving diabetic cataract.
Indexed as
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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 Socratic graph.