Related Experiment Video

Updated: May 14, 2026

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
06:43

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.

Cardiovascular Pathology : the Official Journal of the Society for Cardiovascular Pathology
|February 5, 2013
PubMed

Insights

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.

Keywords:
AtherosclerosisFibrosisPathogenesisRisk factorsSignal transduction

More Related Videos

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation08:43

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Published on: May 31, 2016

Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression13:07

Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression

Published on: January 15, 2022

Related Concept Videos

Atherosclerosis I: Introduction01:30

Atherosclerosis I: Introduction

Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
Venous Thrombosis I: Introduction01:30

Venous Thrombosis I: Introduction

Venous thrombosis, the most common disorder of the veins, involves the formation of a thrombus or blood clot associated with vein inflammation. It can be classified as either superficial vein thrombosis or deep vein thrombosis.Superficial Vein Thrombosis: This involves the formation of a thrombus in a superficial vein, usually the greater or lesser saphenous vein. Though less severe than deep vein thrombosis (DVT), SVT can lead to complications if untreated.Deep Vein Thrombosis (DVT): This...
Inflammation01:38

Inflammation

Overview
Coronary Artery Disease II: Pathophysiology01:26

Coronary Artery Disease II: Pathophysiology

Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
Vascular Spasm01:16

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...