Research summary
The reformulation of atherosclerosis as an inflammatory disease — rather than bland lipid storage — links risk factors to the cellular and cytokine pathways that drive lesion initiation, progression, and thrombotic complication. Inflammation markers were shown to predict outcomes in acute coronary syndromes independently of myocardial injury, and the synthesis ties LDL retention, endothelial activation, monocyte recruitment, foam-cell formation, and smooth-muscle migration into a single inflammatory continuum extending from the fatty streak through fibrous-cap formation and rupture [1]. A subsequent synthesis updates the cellular mechanisms by which cytokines act as inflammatory messengers, drawing on allograft-arteriopathy models that show inflammation alone can drive arterial hyperplasia independent of traditional risk factors, and links specific cytokines (IL-1, IL-6, TNF) to plaque biology and thrombotic triggers [4]. The "vulnerable plaque to vulnerable patient" consensus expands the framework: rupture-prone plaques are not the only vulnerable lesions, and screening must integrate plaque vulnerability, blood vulnerability (procoagulant state), and myocardial vulnerability (arrhythmia susceptibility) to identify patients at risk before sudden events, given that atherosclerotic cardiovascular disease causes more than 19 million deaths annually and many victims die suddenly without prior symptoms [7]. The JUPITER trial — a randomized, double-blind, placebo-controlled assignment of 17,802 apparently healthy adults with LDL-C below 130 mg/dL but hsCRP at or above 2.0 mg/L to rosuvastatin 20 mg daily versus placebo — provided the prospective clinical demonstration that inflammation-targeted statin therapy reduces vascular events in this previously untreated population [2], with the trial design and inflammatory rationale further summarised in the gynaecology-focused review [5]. A review of diabetes and atherosclerosis integrates epidemiology, endothelial dysfunction, vascular smooth-muscle behaviour, platelet activity, and revascularisation data to address the gap between recognised risk and underused medical therapy in diabetic vascular disease [6]. The Braunwald's Heart Disease textbook consolidates these mechanistic and clinical strands into a working reference covering molecular biology, imaging, pharmacology, interventional cardiology, and electrophysiology [3].
Recent publications
- Inflammation in atherosclerosisDOI
- Inflammation and AtherosclerosisDOI
- Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive ProteinDOI
- Progress and challenges in translating the biology of atherosclerosisDOI
- Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine
- Inflammation in AtherosclerosisDOI
- Rosuvastatin to Prevent Vascular Events in Men and Women With Elevated C-Reactive ProteinDOI
- AtherosclerosisDOI
- Diabetes and AtherosclerosisDOI
- From Vulnerable Plaque to Vulnerable PatientDOI
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External profiles
- ORCID: https://orcid.org/0000-0002-1502-502X
- OpenAlex: openalex.org
Profile compiled from public sources (Researchmap, OpenAlex, Osaka University faculty directory). Last refreshed 2026-05. Report incorrect information.