ReviewFrontiers in cardiovascular medicine2025
The "angiogenesis-plaque stability paradox" in atherosclerosis pathogenesis.
Review in Frontiers in cardiovascular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed.
- Mouse Models of Atherosclerosis: What They Teach Us, What They Miss, and When to Use Them.Bioengineering (Basel, Switzerland) · 2026Review
- T‑cadherin and its impact on human diseases (Review).Molecular medicine reports · 2026Review
- Plasma levels of soluble Flt-1 and Tie-2 correlate with neovascularization in human carotid atherosclerotic plaques - a pilot study.Frontiers in immunology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intraplaque angiogenesis, a critical mechanism in the pathological progression of atherosclerosis (AS), exhibits a paradoxical role by providing nutrients and repair support for plaques while simultaneously contributing to plaque instability and rupture. Current research on intraplaque angiogenesis primarily focuses on molecular mechanisms, cellular interactions, and metabolic regulation; however, its dual effects on plaque stability remain underexplored. This review elucidates the mechanisms underlying the angiogenesis-plaque stability paradox, including the glycolysis-lactate-lactylation modification axis, mast cell-mediated inflammatory responses, and angiogenic maturation and stabilization mechanisms, and discusses their roles and associated regulatory pathways in AS pathogenesis. These insights aim to potentiate atherosclerotic plaque stabilization and refine predictive accuracy for acute cardiovascular events.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.