ArticleCells2025
Type 2 Diabetes Mellitus Impairs the Reverse Transendothelial Migration Capacity (rTEM) of Inflammatory CD14
Article in Cells, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Diagnostic value of systemic immune-inflammation composite index combined with triglyceride-glucose index in type 2 diabetes patients with coronary heart disease: a retrospective diagnostic model study.BMC cardiovascular disorders · 2026Article
- Differences in Neurofilament Light Chain, Glial Fibrillary Acidic Protein, and Tau Protein Levels in Patients with Temporal Lobe Epilepsy and Comorbid Depression.Molecular neurobiology · 2026Article
- Flow-based imaging reveals dissociated monocyte adhesion and transmigration patterns between TNF-α and diabetes-induced vascular inflammation.Frontiers in immunology · 2026Article
- Umbelliferone reverses neuronal damage induced by chronic Chlorpyrifos exposure via suppressing NF-κB/STAT3/NLRP3 and boosting Keap-1/Nrf2/HO-1 signals.Metabolic brain disease · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundType 2 diabetes mellitus (DM) is a major cardiovascular risk factor that induces monocyte dysfunction and contributes to their accumulation in atherosclerotic lesions. Monocyte recruitment and accumulation in the tissues contribute to chronic inflammation and are essential to the pathobiology of diabetes-induced atherosclerosis. However, the mechanisms that drive the accumulation of monocytes in the diabetic environment are not clearly understood.
methodsPrimary monocytes from type 2 (T2) DM and non-T2DM individuals were isolated using magnet-assisted cell sorting. To examine the influence of a diabetic milieu on monocyte function, monocytes from T2DM patients, db/db mice, or human monocytes subjected to hyperglycaemia were analysed for their responses to pro-atherogenic cytokines using Boyden chamber assays. Furthermore, the interactions of non-diabetic and diabetic monocytes with TNFα-inflamed endothelium were studied using live-cell imaging under physiological flow conditions. RT-qPCR and FACS were used to study the expression of relevant molecules involved in monocyte-endothelium interaction.
resultsCD14
conclusionsOur results revealed for the first time that the enhanced T2DM monocyte accumulation in the ablumen is not secondary to the elevated transmigration through the endothelium. Instead, the accumulation of monocytes is due to the direct consequence of a dysfunctional rTEM, potentially due to enhanced JAM3-MAC1 engagement. Our results highlight the importance of restoring the rTEM capacity of monocytes to reduce monocyte accumulation-dependent inflammation induction and atherogenesis in the T2DM environment.
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