Reactive oxygen species mediates a metabolic memory of high glucose stress signaling in bovine retinal pericytes

Zhang, Liwei; Zhao, Han; Chen, Bai-hua

doi:10.18240/ijo.2019.07.03

Cited by 4 publications

(4 citation statements)

References 31 publications

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“…and preventing mitochondrial dysfunction [58]. In DM, decreased MnSOD levels may lead to increased ROS levels and play a critical role in pericyte loss of DR [59].…”

Section: Mtdna-related Methylationmentioning

confidence: 99%

DNA methylation in diabetic retinopathy: pathogenetic role and potential therapeutic targets

Cai

Meng

et al. 2022

Cell Biosci

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Background Diabetic retinopathy (DR), a specific neuron-vascular complication of diabetes, is a major cause of vision loss among middle-aged people worldwide, and the number of DR patients will increase with the increasing incidence of diabetes. At present, it is limited in difficult detection in the early stages, limited treatment and unsatisfactory treatment effects in the advanced stages. Main body The pathogenesis of DR is complicated and involves epigenetic modifications, oxidative stress, inflammation and neovascularization. These factors influence each other and jointly promote the development of DR. DNA methylation is the most studied epigenetic modification, which has been a key role in the regulation of gene expression and the occurrence and development of DR. Thus, this review investigates the relationship between DNA methylation and other complex pathological processes in the development of DR. From the perspective of DNA methylation, this review provides basic insights into potential biomarkers for diagnosis, preventable risk factors, and novel targets for treatment. Conclusion DNA methylation plays an indispensable role in DR and may serve as a prospective biomarker of this blinding disease in its relatively early stages. In combination with inhibitors of DNA methyltransferases can be a potential approach to delay or even prevent patients from getting advanced stages of DR.

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“…and preventing mitochondrial dysfunction [58]. In DM, decreased MnSOD levels may lead to increased ROS levels and play a critical role in pericyte loss of DR [59].…”

Section: Mtdna-related Methylationmentioning

confidence: 99%

DNA methylation in diabetic retinopathy: pathogenetic role and potential therapeutic targets

Cai

Meng

et al. 2022

Cell Biosci

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“…Several therapeutic approaches have been assessed targeting mitochondrial dysfunction despite the low specificity of DNMT, synthetic DNA methylation inhibitors such as hydralazine and procainamide are being evaluated in clinical trials, or polyphenols like resveratrol have shown to directly inhibit DNMTs as well as being a powerful antioxidant which ultimately lead to epigenetic changes with altered gene expression [251][252][253][254].…”

Section: Dna Methylationmentioning

confidence: 99%

“…Therefore, this makes us think that the regulation of biogenesis by pharmaceutical or molecular means could provide a way to prevent the development/progression of DR [261]. Examples of these are approaches with intravitreal adeno associated viral MnSOD which showed to reduce retinal capillary basement membrane thickness, inhibit apoptosis of these capillaries, by effectively overexpressing MnSOD, suggesting an ameliorative effect on the metabolic memory phenomenon [254,262]. Moreover, different approaches have been made with different polyphenols, the most promising one is resveratrol that is associated with decreased phosphorylation of 5'-adenosine monophosphate activated protein kinase (AMPK) that regulates histone deacetylase Sirtuin 1 (Sirt1) which may ultimately suppress NF-kB activation [252].…”

Section: Modification Of Histonesmentioning

confidence: 99%

Importance of the Use of Oxidative Stress Biomarkers and Inflammatory Profile in Aqueous and Vitreous Humor in Diabetic Retinopathy

et al. 2020

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Diabetic retinopathy is one of the leading causes of visual impairment and morbidity worldwide, being the number one cause of blindness in people between 27 and 75 years old. It is estimated that ~191 million people will be diagnosed with this microvascular complication by 2030. Its pathogenesis is due to alterations in the retinal microvasculature as a result of a high concentration of glucose in the blood for a long time which generates numerous molecular changes like oxidative stress. Therefore, this narrative review aims to approach various biomarkers associated with the development of diabetic retinopathy. Focusing on the molecules showing promise as detection tools, among them we consider markers of oxidative stress (TAC, LPO, MDA, 4-HNE, SOD, GPx, and catalase), inflammation (IL-6, IL-1ß, IL-8, IL-10, IL-17A, TNF-α, and MMPs), apoptosis (NF-kB, cyt-c, and caspases), and recently those that have to do with epigenetic modifications, their measurement in different biological matrices obtained from the eye, including importance, obtaining process, handling, and storage of these matrices in order to have the ability to detect the disease in its early stages.

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“…The long time preservation of a certain epigenetic writing, translates in the cellular ability to retain phenotypic and behavioral traits, typical of the donor organism from which they originated. This concept explains, for instance, why cultured cells irrespective to the number of passages and culturing conditions, preserve representative qualities of the donors’ pathology, as it is the case for fibroblasts and endothelial cells derived from diabetic subjects [ 17 , 18 , 19 , 20 , 21 ].…”

Section: Introductionmentioning

confidence: 99%

Cell-Free Filtrates (CFF) as Vectors of a Transmissible Pathologic Tissue Memory Code: A Hypothetical and Narrative Review

Berlanga‐Acosta

Fernández‐Mayola

Mendoza‐Marí

et al. 2022

IJMS

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Cellular memory is a controversial concept representing the ability of cells to “write and memorize” stressful experiences via epigenetic operators. The progressive course of chronic, non-communicable diseases such as type 2 diabetes mellitus, cancer, and arteriosclerosis, is likely driven through an abnormal epigenetic reprogramming, fostering the hypothesis of a cellular pathologic memory. Accordingly, cultured diabetic and cancer patient-derived cells recall behavioral traits as when in the donor’s organism irrespective to culture time and conditions. Here, we analyze the data of studies conducted by our group and led by a cascade of hypothesis, in which we aimed to validate the hypothetical existence and transmissibility of a cellular pathologic memory in diabetes, arteriosclerotic peripheral arterial disease, and cancer. These experiments were based on the administration to otherwise healthy animals of cell-free filtrates prepared from human pathologic tissue samples representative of each disease condition. The administration of each pathologic tissue homogenate consistently induced the faithful recapitulation of: (1) Diabetic archetypical changes in cutaneous arterioles and nerves. (2) Non-thrombotic arteriosclerotic thickening, collagenous arterial encroachment, aberrant angiogenesis, and vascular remodeling. (3) Pre-malignant and malignant epithelial and mesenchymal tumors in different organs; all evocative of the donor’s tissue histopathology and with no barriers for interspecies transmission. We hypothesize that homogenates contain pathologic tissue memory codes represented in soluble drivers that “infiltrate” host’s animal cells, and ultimately impose their phenotypic signatures. The identification and validation of the actors in behind may pave the way for future therapies.

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Reactive oxygen species mediates a metabolic memory of high glucose stress signaling in bovine retinal pericytes

Cited by 4 publications

References 31 publications

DNA methylation in diabetic retinopathy: pathogenetic role and potential therapeutic targets

DNA methylation in diabetic retinopathy: pathogenetic role and potential therapeutic targets

Importance of the Use of Oxidative Stress Biomarkers and Inflammatory Profile in Aqueous and Vitreous Humor in Diabetic Retinopathy

Cell-Free Filtrates (CFF) as Vectors of a Transmissible Pathologic Tissue Memory Code: A Hypothetical and Narrative Review

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