Type 2 Diabetes Mellitus Impairs the Reverse Transendothelial Migration Capacity (rTEM) of Inflammatory CD14+CD16− Monocytes: Novel Mechanism for Enhanced Subendothelial Monocyte Accumulation in Diabetes

Our 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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Journal
Cells
Published
2025-10-09
DOI
https://doi.org/10.3390/cells14191567
Citations
1
Primary Topic
Atherosclerosis and Cardiovascular Diseases
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article
Field-Weighted Citation Impact
0.80
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article

Type 2 Diabetes Mellitus Impairs the Reverse Transendothelial Migration Capacity (rTEM) of Inflammatory CD14+CD16− Monocytes: Novel Mechanism for Enhanced Subendothelial Monocyte Accumulation in Diabetes

Johannes Waltenberger, Dilvin Semo, Beat A. Imhof, Adama Sidibé et al.
1 citations
Cells
Atherosclerosis and Cardiovascular Diseases
0.80
article

Type 2 Diabetes Mellitus Impairs the Reverse Transendothelial Migration Capacity (rTEM) of Inflammatory CD14+CD16− Monocytes: Novel Mechanism for Enhanced Subendothelial Monocyte Accumulation in Diabetes

Johannes Waltenberger, Dilvin Semo, Beat A. Imhof, Adama Sidibé, Rinesh Godfrey, Kallipatti Sanjith Shanmuganathan, N Müller, Ulrich Müller
article en
1 citations

Abstract

Our 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.

CellsVol. 14(19)
University of Geneva (CH), University of Münster (DE), Maastricht University (NL), Hirslanden Klinik Im Park (CH), University Hospital Münster (DE), Jena University Hospital (DE), Clinical Research Center Kiel (DE)
Openalex Percentile: Top 23%
Atherosclerosis and Cardiovascular Diseases
0.80
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Type 2 Diabetes Mellitus Impairs the Reverse Transendothelial Migration Capacity (rTEM) of Inflammatory CD14+CD16− Monocytes: Novel Mechanism for Enhanced Subendothelial Monocyte Accumulation in Diabetes — Johannes Waltenberger, Dilvin Semo, et al. · Cells (2025) | TGRS Research Map | TGRS