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Updated: May 14, 2026
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Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
Published on: December 7, 2013
Vascular fibrosis in atherosclerosis
Tao-Hua Lan1, Xiong-Qing Huang, Hong-Mei Tan
1Department of Pathophysiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, PR China; Department of Cardiology, Guangdong Provincial Hospital of Chinese Medicine (postdoctoral mobile research station of Guangzhou University of Traditional Chinese Medicine), Guangzhou, 510006, PR China.
Summary
Vascular fibrosis, marked by arterial thickening and reduced lumen, is driven by excessive matrix deposition. Key mediators like RAAS, TGF-beta, and MMPs/TIMPs imbalance contribute to this atherosclerosis progression.
Area of Science:
- Cardiovascular Biology
- Pathophysiology
- Vascular Medicine
Background:
- Vascular fibrosis, characterized by arterial wall thickening and lumen narrowing due to excessive extracellular matrix (ECM) deposition, is a key pathological process in atherosclerosis.
- Risk factors for cardiovascular disease such as hypertension and dyslipidemia are implicated in the initiation and progression of vascular fibrosis.
- Vascular fibrosis involves vascular smooth muscle cell (VSMC) proliferation, ECM accumulation, and impaired matrix degradation.
Purpose of the Study:
- To review the pathogenesis of vascular fibrosis in atherosclerosis.
- To highlight the networking among key mediators involved in vascular fibrosis.
- To discuss the main pathophysiologic factors contributing to vascular fibrosis.
Main Methods:
- Literature review focusing on the pathophysiology of vascular fibrosis.
- Analysis of the roles of major mediators including RAAS, TGF-beta, MMPs/TIMPs, and PPAR gamma.
- Discussion of the interconnections between these factors in vascular remodeling.
Main Results:
- Vascular fibrosis is linked to the renin-angiotensin-aldosterone system (RAAS), oxidative stress, inflammation, growth factors, and endothelial dysfunction.
- Angiotensin II (Ang II) and aldosterone are key RAAS hormones driving vascular fibrosis.
- Transforming growth factor-beta (TGF-beta) promotes ECM accumulation, while an imbalance between matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) leads to collagen deposition.
Conclusions:
- Understanding the networking among mediators like RAAS, TGF-beta, and MMPs/TIMPs is crucial for addressing vascular fibrosis in atherosclerosis.
- Aberrant expression of factors such as peroxisome proliferator-activated receptor gamma (PPAR gamma) also contributes to pathological fibrosis and vascular remodeling.
- This review synthesizes current knowledge on the pathogenesis of vascular fibrosis, emphasizing its complex multifactorial nature.
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