[Basic research of fibrosis on atherosclerotic plaque stability and related drug application]

Area of Science:

• Cardiovascular Medicine
• Pathology
• Pharmacology

Background:

• Cardiovascular diseases (CVDs) exhibit high incidence and mortality.
• Atherosclerosis is the primary pathological feature and progression basis for CVDs.
• Unstable plaque rupture, shedding, and thrombosis are critical, dangerous events in plaque evolution.

Purpose of the Study:

• To clarify atherosclerotic plaque development.
• To explain the roles of inflammatory cells and cytokines in plaque stability.
• To review recent drug research for plaque stabilization.

Main Methods:

• Literature review and analysis of inflammatory and fibrotic processes in atherosclerosis.
• Examination of the relationship between inflammation, fibrosis, and plaque stability.
• Summary of current drug development strategies targeting plaque stabilization.

Main Results:

• Plaque fibrosis is identified as the core mechanism regulating atherosclerotic plaque stability.
• Fibrosis dynamically reflects inflammatory and pathological changes within plaques.
• Inflammatory cells and cytokines play significant roles in modulating plaque stability.

Conclusions:

• Improving plaque fibrosis is a novel therapeutic approach for stabilizing atherosclerotic plaques.
• Targeting fibrosis holds promise for future drug development in atherosclerosis treatment.
• Understanding inflammation-fibrosis interplay is crucial for managing CVDs.