ArticleExperimental eye research2010
Metabolic memory and diabetic retinopathy: role of inflammatory mediators in retinal pericytes.
Article in Experimental eye research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 78 citations in OpenAlex.
- Association of systemic inflammatory indices and body mass index with diabetic macular edema in non-proliferative diabetic retinopathy.BMC ophthalmology · 2026Article
- Pericytes as key mediators of microenvironmental signaling crosstalk: implications in vascular diseases and cancer.Frontiers in cell and developmental biology · 2026Review
- Metabolic memory in diabetic complications: evidence for persistent cellular states and limits of therapeutic reversal.Frontiers in endocrinology · 2026Review
- Wnt/β-Catenin Signaling in Diabetic Complications: Mechanisms and Therapeutic Potential.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- MicroRNAs in diabetes mellitus.Journal of diabetes and metabolic disorders · 2025Review
- Intravitreal therapy for the management of diabetic retinopathy: A concise review.World journal of experimental medicine · 2024Review
- Induction, amplification, and propagation of diabetic retinopathy-associated inflammatory cytokines between human retinal microvascular endothelial and Müller cells and in the mouse retina.Cellular signalling · 2024Article
- Update: the role of epigenetics in the metabolic memory of diabetic complications.American journal of physiology. Renal physiology · 2024Review
- Mitochondrial Quality Control and Metabolic Memory Phenomenon Associated with Continued Progression of Diabetic Retinopathy.International journal of molecular sciences · 2023Article
- Epigenetic modifications in metabolic memory: What are the memories, and can we erase them?American journal of physiology. Cell physiology · 2022Review
- Biological age and environmental risk factors for dementia and stroke: Molecular mechanisms.Frontiers in aging neuroscience · 2022Review
- Inflammatory mediators in diabetic retinopathy: Deriving clinicopathological correlations for potential targeted therapy.Indian journal of ophthalmology · 2021Review
- Review
- Does epigenetics have a role in age related macular degeneration and diabetic retinopathy?Genes & diseases · 2021Review
- Fenofibrate Protects Cardiomyocytes from Hypoxia/Reperfusion- and High Glucose-Induced Detrimental Effects.PPAR research · 2021Article
- Pyroptosis in the Retinal Neurovascular Unit: New Insights Into Diabetic Retinopathy.Frontiers in immunology · 2021Review
- Pericytes, inflammation, and diabetic retinopathy.Inflammopharmacology · 2020Review
- African and Asian Mitochondrial DNA Haplogroups Confer Resistance Against Diabetic Stresses on Retinal Pigment Epithelial Cybrid Cells In Vitro.Molecular neurobiology · 2020Article
- Astragalus polysaccharides suppresses high glucose-induced metabolic memory in retinal pigment epithelial cells through inhibiting mitochondrial dysfunction-induced apoptosis by regulating miR-195.Molecular medicine (Cambridge, Mass.) · 2019Article
- Targeting human 8-oxoguanine DNA glycosylase to mitochondria protects cells from high glucose-induced apoptosis.Endocrine · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Diabetic retinopathy shares many characteristics features of a low grade chronic inflammatory disease. Its progression resists arrest when good metabolic control is re-established after a period of poor metabolic control, suggesting a 'metabolic memory' phenomenon. The aim of this study is to investigate the effect of reversal of high glucose to normal glucose on the inflammatory mediators in pericytes, the site of histopathology in diabetic retinopathy. Bovine retinal pericytes were incubated in high glucose (20 mM) for 2 days followed by normal glucose (5 mM) for 4 days (2 --> 4), or in high glucose for 4 days followed by normal glucose for 4 days (4 --> 4) or 8 days (4 --> 8). Pericytes incubated in continuous normal or high glucose for 2-12 days served as controls. Continuous high glucose exposure for 2-12 days significantly elevated gene expressions and protein concentrations of IL-1 beta, NF-kB, VEGF, TNF-alpha, TGF-beta and ICAM-1 in retinal pericytes. Four days of normal glucose that followed 2 days of high glucose (2 --> 4) had marginal, but significant, beneficial effect on the increases in these inflammatory mediators. Four days of normal glucose in 4 --> 4 group failed to reverse increases in inflammatory mediators and cell apoptosis remained elevated, but addition of dexamethasone during normal glucose exposure ameliorated such increases. However, when normal glucose exposure, after 4 days of high glucose was extended to 8 days (4 --> 8), increases in these mediators were significantly decreased. Hyperglycemia-induced elevations in inflammatory mediators in retinal microvascular cells resist reversal after re-institution of normal glucose conditions. Both, the duration of the initial exposure to high glucose, and normal glucose that follows high glucose, are critical in determining the outcome of the alterations in the inflammatory mediators.
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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 OpenQuestion graph.