Key result
Desialylated LDL drives atherogenicity by promoting intracellular lipid accumulation and autoimmune responses.
Why the study?
The atherogenic effects and contribution to atherogenicity of desialylated LDL are often underestimated or forgotten.
Answers are grounded in this paper and cite their sources.
This review highlights the often-underestimated role of lipoprotein desialylation in atherogenesis and suggests targeting sialidase activity as a potential future therapeutic strategy for atherosclerosis.
Atherosclerosis is one of the leading causes of death in developed and developing countries. The atherogenicity phenomenon cannot be separated from the role of modified low-density lipoproteins (LDL) in atherosclerosis development. Among the multiple modifications of LDL, desialylation deserves to be discussed separately, since its atherogenic effects and contribution to atherogenicity are often underestimated or, simply, forgotten. Vladimir Tertov is linked to the origin of the research related to desialylated lipoproteins, including the association of modified LDL with atherogenicity, autoimmune nature of atherosclerosis, and discovery of sialidase activity in blood plasma. The review will briefly discuss all the above-mentioned information, with a description of the current situation in the research.
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Glanz et al. (2022) conducted a review in Atherosclerosis. Desialylated lipoproteins was evaluated. Desialylated low-density lipoproteins contribute significantly to atherogenicity by promoting intracellular lipid accumulation and initiating autoimmune responses in atherosclerosis.
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