Research
Macro partitioning
Atherogenesis is fundamentally driven by the accumulation of oxidatively modified LDL in the arterial intima, facilitated by endothelial dysfunction and scavenger receptor uptake by macrophages to form foam cells.
High LDL cholesterol is a primary cause of atherosclerosis. The risk is highest when LDL is oxidized and taken up by macrophages to form foam cells. Managing LDL levels and reducing oxidative stress are key to preventing plaque buildup.
StrongSupportsVERY_HIGH confidence
Atherogenesis is mediated in large part by the endothelium causing inflammation and accumulation of oxidatively modified LDL in the intima of the vessel wall facilitating monocyte recruitment and foam cell formation.
Why this rating
Described as an 'undeniable causal relationship' with extensive mechanistic detail on LDL modification and foam cell formation.
Source
Atherosclerosis: Pathophysiology of insulin resistance, hyperglycemia, hyperlipidemia, and inflammation
Joshua Beverly et al. · Journal of Diabetes · 2019
DOI 10.1111/1753-0407.12970
narrative_reviewCited 220×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Insulin resistance promotes atherosclerosis through impaired insulin signaling (specifically reduced PI-3 kinase activation) which decreases nitric oxide production, leading to endothelial dysfunction and accelerated plaque progression, independent of hyperglycemia.Good
- Chronic hyperglycemia accelerates atherosclerosis through three distinct mechanisms: formation of advanced glycation end products (AGEs) that modify LDL, increased oxidative stress reducing nitric oxide, and pathologic activation of Protein Kinase C (PKC).Good
- Inflammation is involved in every step of the atherosclerotic process, from initial lipid retention to plaque destabilization, mediated by both innate (macrophages, TLRs) and adaptive (T cells, B cells) immune responses.Good
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