12/26/2023 0 Comments Abscissa international inc.In type 2 diabetes (T2D) patients with reduced glomerular endothelial fenestrae, albuminuria and a drop in glomerular filtration rate (GFR) are significantly connected ( 18– 21). In this sense, the underlying mechanisms of hyperglycemic injury for microvascular endothelial cells require further investigation. Additionally, the systemic inflammation induced by the albuminuria-impaired kidney is considered to accelerate the clinical course of microvascular complications in both the eye and the kidney ( 11– 17). The polyol pathway is involved in the development of the two disorders, as are increased advanced glycation end products (AGEs) synthesis, increased expression of the AGE receptor and its activating ligands, activation of protein kinase C isoforms, overactivity of the hexosamine pathway, and other pathways ( 8– 10). As an important structural and overlapping determinant of disease development, the relationship between kidney disease and retinal disease has been discussed, and the term “renal-retinal syndrome” has been recognized by the public ( 6, 7). It is recognized that retinopathy and nephropathy occur simultaneously in long-term diabetes. According to the epidemiological type-2 diabetes surveys in Chinese major cities, DN and DR account for 39.7% and 31.5% of diabetic microangiopathy, respectively ( 4). High blood sugar level is considered to induce the microvascular endothelial dysfunction in which diabetic nephropathy (DN) and diabetic retinopathy (DR) are the most common disorders. Because their failure to downregulate the glucose transport rate results in intracellular hyperglycemia when glucose levels are high, microvascular endothelial cells are regarded to be the major targets of hyperglycemic damage ( 4, 5). The major lethal causes for diabetic patients are diabetic macrovascular and microvascular complications that are derived from the diabetes-induced endothelial dysfunction. Diabetes’ global occurrence has risen substantially from 108 million in 1980 to 422 million in 2014, according to epidemiological data, and diabetes is anticipated to become the seventh leading cause of death by 2030 ( 1– 4). Bioinformatics analysis pointed to an important role in reducing excess cysteine and methionine metabolism.Ĭonclusion: FIBA overexpression and 1-MH loss may be linked to the pathogenicity of diabetic endothelial dysfunction in DR/DN, implying that a cohort study is needed to further investigate the role of FIBA and 1-MH in the development of DN and DR, as well as the related pathways between the two proteins.ĭiabetes has become much more common during the last few decades all throughout the world. Results: It can be assumed that serum exosomes extracted by DRDN patients might cause endothelial dysfunction mainly by upregulating alpha subunit of the coagulation factor fibrinogen (FIBA) and downregulating 1-methylhistidine (1-MH). Metabolomics ultraperformance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) and proteomics tandem mass tag (TMT)-based liquid chromatography-tandem mass spectrometry (LC-MS/MS) together with bioinformatics, the correlation analysis, and the joint pathway analysis were employed to discover the underlying mechanisms of endothelial dysfunction caused by patient’s SExos. Methods: In this study, human glomerular endothelial cells (HGECs) were used as the cell model. Microvascular endothelial cells are thought to be major targets of hyperglycemic damage, while the underlying mechanism of diffuse endothelial dysfunction in multiple organs needs to be further investigated.Īim: The aim of this study is to explore the endothelial dysfunction mechanisms of serum exosomes (SExos) extracted from DR and DN (DRDN) patients. 5Department of Integrated Traditional and Western Nephrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Chinaīackground: The prevalence of diabetic microvascular diseases has increased significantly worldwide, the most common of which are diabetic nephropathy (DN) and diabetic retinopathy (DR).4Key Laboratory of Precision Diagnosis and Treatment of Chronic Kidney Disease in Henan Province, Zhengzhou, China.3Henan Province Research Center for Kidney Disease, Zhengzhou, China.2Research Institute of Nephrology, Zhengzhou University, Zhengzhou, China.1Department of Ophthalmology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
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