Why the study?
Understanding how focal atherosclerotic lesions form in the vascular wall remains incomplete because discussions usually focus on stages after low-density lipoproteins have already entered the intima.
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Design
Review
Transcytosis mechanisms may clarify early LDL infiltration in atherosclerosis; leaves open targeted validation before any practice implications.
Understanding how focal atherosclerotic lesions are formed in the vascular wall currently remains clearly incomplete, and primarily because the discussion of this issue is usually considered at the stage when low-density lipoproteins are already in the intima; the situation is largely clarified if attention is paid primarily to the mechanisms of intima infiltration by lipoproteins. From the modern point of view, we are talking about the molecular mechanisms of transcytosis, previously detected by the electron microscopy on endothelial cells of rat capillaries, which were injected with gold or ferritin nanoparticles to trace their path in the cytoplasm. Transcytosis as an active process, in which a number of receptors are involved, is contrasted with passive lipoproteins infiltration of the vascular wall. In addition to these concepts, the review discusses possible conditions for the implementation of low-density lipoproteins transcytosis, as well as the issues of regulation of transcytosis.
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Ns et al. (2023) studied this question.
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