# The “angiogenesis-plaque stability paradox” in atherosclerosis pathogenesis

## TL;DR

This review explores how blood vessel growth in atherosclerotic plaques both supports and destabilizes them, aiming to improve understanding and treatment of heart disease.

## Contribution

The paper introduces a novel framework for understanding the dual role of angiogenesis in plaque stability through specific molecular and cellular mechanisms.

## Key findings

- The glycolysis-lactate-lactylation axis plays a key role in the angiogenesis-plaque stability paradox.
- Mast cell-mediated inflammation contributes to plaque instability through angiogenesis.
- Angiogenic maturation and stabilization mechanisms influence atherosclerosis progression.

## 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.