REVIEW article
Front. Cardiovasc. Med.
Sec. Atherosclerosis and Vascular Medicine
Volume 12 - 2025 | doi: 10.3389/fcvm.2025.1659006
This article is part of the Research TopicCardiovascular Mechanobiology: Molecular Mechanisms, Disease Pathogenesis, and Therapeutic OpportunitiesView all articles
The "angiogenesis-plaque stability paradox" in atherosclerosis pathogenesis
Provisionally accepted
- Henan University of Chinese Medicine, Zhengzhou, China
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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.
Keywords: Atherosclerosis, Angiogenesis, plaque stability, Glycolysis, Mast Cells
Received: 03 Jul 2025; Accepted: 19 Sep 2025.
Copyright: © 2025 Yan, sun and wu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: hong wu, kevin5me@126.com
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