Advanced Glycation End Products and Their Effect on Vascular Complications in Type 2 Diabetes Mellitus

Lee, Jeongmin; Yun, Jae‐Seung; Ko, Seung‐Hyun

doi:10.3390/nu14153086

Cited by 53 publications

(32 citation statements)

References 116 publications

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“…The aberrant remodeling of blood vessels brought on by AGEs and their RAGE receptors (AGEs/RAGE axis) leads to vascular complications in patients with diabetes [ 56 ]. Cell line and animal models have both been used to study type 2 diabetes.…”

Section: Discussionmentioning

confidence: 99%

Differentially Expressed Cell Cycle Genes and STAT1/3-Driven Multiple Cancer Entanglement in Psoriasis, Coupled with Other Comorbidities

Anand

2022

Cells

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Psoriasis is a persistent T-cell-supported inflammatory cutaneous disorder, which is defined by a significant expansion of basal cells in the epidermis. Cell cycle and STAT genes that control cell cycle progression and viral infection have been revealed to be comorbid with the development of certain cancers and other disorders, due to their abnormal or scanty expression. The purpose of this study is to evaluate the expression of certain cell cycle and STAT1/3 genes in psoriasis patients and to determine the types of comorbidities associated with these genes. To do so, we opted to adopt the in silico methodology, since it is a quick and easy way to discover any potential comorbidity risks that may exist in psoriasis patients. With the genes collected from early research groups, protein networks were created in this work using the NetworkAnalyst program. The crucial hub genes were identified by setting the degree parameter, and they were then used in gene ontology and pathway assessments. The transcription factors that control the hub genes were detected by exploring TRRUST, and DGIdb was probed for remedies that target transcription factors and hubs. Using the degree filter, the first protein subnetwork produced seven hub genes, including STAT3, CCNB1, STAT1, CCND1, CDC20, HSPA4, and MAD2L1. The hub genes were shown to be implicated in cell cycle pathways by the gene ontology and Reactome annotations. The former four hubs were found in signaling pathways, including prolactin, FoxO, JAK/STAT, and p53, according to the KEGG annotation. Furthermore, they enhanced several malignancies, including pancreatic cancer, Kaposi’s sarcoma, non-small cell lung cancer, and acute myeloid leukemia. Viral infections, including measles, hepatitis C, Epstein–Barr virus, and HTLV-1 and viral carcinogenesis were among the other susceptible diseases. Diabetes and inflammatory bowel disease were conjointly annotated. In total, 129 medicines were discovered in DGIdb to be effective against the transcription factors BRCA1, RELA, TP53, and MYC, as opposed to 10 medications against the hubs, STAT3 and CCND1, in tandem with 8 common medicines. The study suggests that the annotated medications should be tested in suitable psoriatic cell lines and animal models to optimize the drugs used based on the kind, severity, and related comorbidities of psoriasis. Furthermore, a personalized medicine protocol must be designed for each psoriasis patient that displays different comorbidities.

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Section: Discussionmentioning

confidence: 99%

Differentially Expressed Cell Cycle Genes and STAT1/3-Driven Multiple Cancer Entanglement in Psoriasis, Coupled with Other Comorbidities

Anand

2022

Cells

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“…Likewise, advanced glycosylation end products (AGEs) further promote ROS production, induce overexpression of endothelial angiopoietin (Ang)-2, promote cellular sensitivity to pro-inflammatory factors such as vascular cell-adhesion molecule (VCAM)-1, and contribute to the progression of diabetes-related vascular disease ( 46 ). AGEs are non-enzymatic glycosylated forms of free amino acids that result from the interaction of glucose with lipids or proteins, bind to receptors to promote inflammation and oxidative stress, and are important in contributing to glomerulosclerosis and mesangial hypertrophy in DKD ( 47 – 49 ). On the other hand, ROS acts as an agonist of NF-κB signaling pathway to initiate the activation of downstream inflammatory signaling pathways and promotes the release of inflammatory factors such as IL-1β, TNF-α, intercellular adhesion molecule-1 (ICAM-1) and monocyte chemotactic protein-1 (MCP-1) ( 50 – 54 ).…”

Section: Oxidative Stress and Rosmentioning

confidence: 99%

The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications

et al. 2023

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Diabetes mellitus (DM) is a metabolic disease characterized by chronic hyperglycaemia, with absolute insulin deficiency or insulin resistance as the main cause, and causes damage to various target organs including the heart, kidney and neurovascular. In terms of the pathological and physiological mechanisms of DM, oxidative stress is one of the main mechanisms leading to DM and is an important link between DM and its complications. Oxidative stress is a pathological phenomenon resulting from an imbalance between the production of free radicals and the scavenging of antioxidant systems. The main site of reactive oxygen species (ROS) production is the mitochondria, which are also the main organelles damaged. In a chronic high glucose environment, impaired electron transport chain within the mitochondria leads to the production of ROS, prompts increased proton leakage and altered mitochondrial membrane potential (MMP), which in turn releases cytochrome c (cyt-c), leading to apoptosis. This subsequently leads to a vicious cycle of impaired clearance by the body’s antioxidant system, impaired transcription and protein synthesis of mitochondrial DNA (mtDNA), which is responsible for encoding mitochondrial proteins, and impaired DNA repair systems, contributing to mitochondrial dysfunction. This paper reviews the dysfunction of mitochondria in the environment of high glucose induced oxidative stress in the DM model, and looks forward to providing a new treatment plan for oxidative stress based on mitochondrial dysfunction.

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“…Currently, an estimated 537 million people are at an increased risk of type 2 DM, and this number is expected to increase to 592 million by 2035 and reach 783 million by 2045 1,2 . Type 2 DM patients can develop various complications, including cardiovascular disease, stroke, foot ulcers, chronic kidney failure, and diabetic retinopathy, 3–10 making it one of the world's most critical health concerns 11,12 . Type 2 DM is a multifactorial condition characterized by high blood glucose levels (hyperglycemia), 13–15 which are influenced by genetic and epigenetic factors 16–19 .…”

Section: Introductionmentioning

confidence: 99%

Decreased Alu methylation in type 2 diabetes mellitus patients increases HbA1c levels

Thongsroy,

Mutirangura

2023

Clinical Laboratory Analysis

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IntroductionAlu hypomethylation is a common epigenetic process that promotes genomic instability with aging phenotypes, which leads to type 2 diabetes mellitus (type 2 DM). Previously, our results showed significantly decreased Alu methylation levels in type 2 DM patients. In this study, we aimed to investigate the longitudinal changes in Alu methylation levels in these patients.ResultsWe observed significantly decreased Alu methylation levels in type 2 DM patients compared with normal (p = 0.0462). Moreover, our findings demonstrated changes in Alu hypomethylation over a follow‐up period within the same individuals (p < 0.0001). A reduction in Alu methylation was found in patients with increasing HbA1c levels (p = 0.0013) and directly correlated with increased HbA1c levels in type 2 DM patients (r = −0.2273, p = 0.0387).ConclusionsAlu methylation in type 2 DM patients progressively decreases with increasing HbA1c levels. This observation suggests a potential association between Alu hypomethylation and the underlying molecular mechanisms of elevated blood glucose. Furthermore, monitoring Alu methylation levels may serve as a valuable biomarker for assessing the clinical outcomes of type 2 DM.

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Advanced Glycation End Products and Their Effect on Vascular Complications in Type 2 Diabetes Mellitus

Cited by 53 publications

References 116 publications

Differentially Expressed Cell Cycle Genes and STAT1/3-Driven Multiple Cancer Entanglement in Psoriasis, Coupled with Other Comorbidities

Differentially Expressed Cell Cycle Genes and STAT1/3-Driven Multiple Cancer Entanglement in Psoriasis, Coupled with Other Comorbidities

The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications

Decreased Alu methylation in type 2 diabetes mellitus patients increases HbA1c levels

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