Research
Hormonal
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.
Inflammation drives every stage of heart disease, from the initial buildup of plaque to the rupture that causes heart attacks. Managing inflammation through lifestyle and potentially targeted therapies is crucial for preventing cardiovascular events, not just lowering cholesterol.
GoodSupportsHIGH confidence
In the past two decades, it has been increasingly recognized that inflammation is involved in every step of the atherosclerotic process.
Why this rating
Supported by extensive immunological mechanisms described, though it is a review.
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
- 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.Strong
- 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
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