ArticleFrontiers in endocrinology2023
Exploring the shared molecular mechanism of microvascular and macrovascular complications in diabetes: Seeking the hub of circulatory system injury.
Article in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 4 citations in OpenAlex.
- New insights into diagnostic values and mechanisms of ferroptosis associated with immune infiltration in diabetic kidney disease.Experimental and therapeutic medicine · 2026Article
- Associations between carotid macrovascular and retinal microvascular alterations in diabetes: Evidence synthesis and implications for risk assessment.Atherosclerosis plus · 2026Review
- Perivascular pathology, not macrovascular complexity, governs glymphatic-related dysfunction in preclinical cerebral small vessel disease.Scientific reports · 2026Article
- Editorial: Endothelial dysfunction in metabolic disorders: mechanisms, biomarkers, and emerging therapeutics.Frontiers in pharmacology · 2026Article
- Causal Effects of Oxidative Stress on Diabetes Mellitus and Microvascular Complications: Insights Integrating Genome-Wide Mendelian Randomization, DNA Methylation, and Proteome.Antioxidants (Basel, Switzerland) · 2024Article
- A Non-Coronary, Peripheral Arterial Atherosclerotic Disease (Carotid, Renal, Lower Limb) in Elderly Patients-A Review: Part I-Epidemiology, Risk Factors, and Atherosclerosis-Related Diversities in Elderly Patients.Journal of clinical medicine · 2024Review
- Peripheral Arterial Disease is Associated with Sensorimotor Peripheral Neuropathy in People with Type 2 Diabetes.Medical journal of the Islamic Republic of Iran · 2024Article
- Article
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
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Abstract
Background: Microvascular complications, such as diabetic retinopathy (DR) and diabetic nephropathy (DN), and macrovascular complications, referring to atherosclerosis (AS), are the main complications of diabetes. Blindness or fatal microvascular diseases are considered to be identified earlier than fatal macrovascular complications. Exploring the intrinsic relationship between microvascular and macrovascular complications and the hub of pathogenesis is of vital importance for prolonging the life span of patients with diabetes and improving the quality of life. Materials and methods: The expression profiles of GSE28829, GSE30529, GSE146615 and GSE134998 were downloaded from the Gene Expression Omnibus database, which contained 29 atherosclerotic plaque samples, including 16 AS samples and 13 normal controls; 22 renal glomeruli and tubules samples from diabetes nephropathy including 12 DN samples and 10 normal controls; 73 lymphoblastoid cell line samples, including 52 DR samples and 21 normal controls. The microarray datasets were consolidated and DEGs were acquired and further analyzed by bioinformatics techniques including GSEA analysis, GO-KEGG functional clustering by R (version 4.0.5), PPI analysis by Cytoscape (version 3.8.2) and String database, miRNA analysis by Diana database, and hub genes analysis by Metascape database. The drug sensitivity of characteristic DEGs was analyzed. Result: A total of 3709, 4185 and 8086 DEGs were recognized in AS, DN, DR, respectively, with 1820, 1666, 888 upregulated and 1889, 2519, 7198 downregulated. GO and KEGG pathway analyses of DEGs and GSEA analysis of common differential genes demonstrated that these significant sites focused primarily on inflammation-oxidative stress and immune regulation pathways. PPI networks show the connection and regulation on top-250 significant sites of AS, DN, DR. MiRNA analysis explored the non-coding RNA upstream regulation network and significant pathway in AS, DN, DR. The joint analysis of multiple diseases shows the common influenced pathways of AS, DN, DR and explored the interaction between top-1000 DEGs at the same time. Conclusion: In the microvascular and macrovascular complications of diabetes, immune-mediated inflammatory response, chronic inflammation caused by endothelial cell activation and oxidative stress are the three links linking atherosclerosis, diabetes retinopathy and diabetes nephropathy together. Our study has clarified the intrinsic relationship and common tissue damage mechanism of microcirculation and circulatory system complications in diabetes, and explored the mechanism center of these two vascular complications. It has far-reaching clinical and social value for reducing the incidence of fatal events and early controlling the progress of disabling and fatal circulatory complications in diabetes.
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