ReviewPharmaceutical biology2026
Protective effects of icariin in atherosclerotic cardiovascular disease: mechanistic basis, post-ischemic protection and translational limitations.
Review in Pharmaceutical biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextIcariin (ICA), a prenylated flavonol glycoside from Epimedii Folium, has been investigated in experimental models relevant to atherosclerosis, myocardial infarction, and ischemic tissue injury.
objectivesThis review evaluates experimental evidence on ICA in atherosclerotic plaque biology, post-myocardial infarction remodeling, myocardial ischemia-reperfusion injury, and cerebral ischemic injury.
methodsPubMed and the Web of Science Core Collection were searched from database inception to 19 August 2026, and studies were selected using predefined eligibility criteria. Targeted searches also covered pharmacokinetics, metabolism, toxicology, botanical source, quality control, formulation, and delivery.
resultsIn atherosclerosis models, ICA reduced endothelial inflammatory activation, macrophage lipid uptake, vascular smooth muscle cell (VSMC) proliferation and migration, and lesion burden. Several mechanistic links were tested using pharmacological or genetic perturbation.
conclusionsFuture studies should quantify parent ICA and active metabolites in diseased tissues while assessing plaque composition and stability in the same experiments, so that vascular effects can be related to measured
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