Key result
High BP drives a ~100% increase in endothelial LDL transport in preclinical models.
Computational modeling demonstrates that larger endothelial gaps, higher LDL concentrations, and elevated blood pressure synergistically increase trans-endothelial LDL transport, highlighting mechanisms of atherosclerosis progression.
Intensive LDL and blood pressure control may limit endothelial LDL transport; extends computational evidence for synergistic effects in atherogenesis.
This study employs dissipative particle dynamics (DPD) to investigate low-density lipoprotein (LDL) transport across the endothelium under varying conditions of endothelial leakiness size, LDL concentration, and blood pressure. The endothelial gap size was found to strongly influence LDL transport efficiency: a 32.24 nm gap permitted approximately 1.2 times more LDL particles to cross than a 28.69 nm endothelial leakiness. Moreover, higher LDL concentrations significantly promoted trans-endothelial movement, with tenfold elevations in LDL levels increasing transport by about 1.6 times compared to baseline. Finally, elevated blood pressure more than doubled the number of LDL particles crossing the endothelium relative to normal pressure. These findings underscore the critical roles of endothelial integrity, lipid homeostasis, and blood pressure in the progression of atherosclerosis. Larger gaps, excessive LDL levels, and hypertension all contribute to heightened LDL infiltration, potentially accelerating plaqu.
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Fan et al. (2026) studied this question. Increasing endothelial gap size from 28.69 to 32.24 nm increased LDL transport by 1.2x; 10-fold LDL rise raised transport 1.6x; high blood pressure more than doubled LDL crossing.
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