The "angiogenesis-plaque stability paradox" in atherosclerosis pathogenesis

Area of Science:

• Cardiovascular Research
• Pathology
• Molecular Biology

Background:

• Atherosclerosis (AS) progression involves intraplaque angiogenesis, a process with dual effects on plaque stability.
• While providing nutrients, intraplaque angiogenesis can also promote plaque instability and rupture.
• Existing research often overlooks the paradoxical impact of angiogenesis on plaque stability.

Purpose of the Study:

• To elucidate the mechanisms behind the angiogenesis-plaque stability paradox in atherosclerosis.
• To explore the roles of the glycolysis-lactate-lactylation axis, mast cell responses, and angiogenic maturation in AS pathogenesis.
• To identify pathways for potentiating plaque stabilization and improving cardiovascular event prediction.

Main Methods:

• Review of current literature on intraplaque angiogenesis in atherosclerosis.
• Analysis of molecular mechanisms, cellular interactions, and metabolic regulation.
• Discussion of regulatory pathways involved in AS pathogenesis.

Main Results:

• The review details the glycolysis-lactate-lactylation axis's contribution to the paradox.
• Mast cell-mediated inflammatory responses are identified as a key factor.
• Mechanisms of angiogenic maturation and stabilization are discussed in relation to plaque stability.

Conclusions:

• Understanding the dual role of intraplaque angiogenesis is crucial for managing atherosclerosis.
• Targeting specific pathways, like glycolysis and inflammation, may stabilize plaques.
• These insights can enhance the accuracy of predicting acute cardiovascular events.