Matrix Metalloproteinases in Venous Tissue Remodeling and Varicose Vein Formation

2008 ◽  
Vol 6 (3) ◽  
pp. 158-172 ◽  
Author(s):  
Joseph Raffetto ◽  
Raouf Khalil
Keyword(s):  
Matrix Metalloproteinases ◽  
Varicose Vein ◽  
Tissue Remodeling ◽  
Vein Formation ◽  
Venous Tissue

Mechanisms of varicose vein formation: valve dysfunction and wall dilation

2008 ◽  
Vol 23 (2) ◽  
pp. 85-98 ◽  
Author(s):  
J D Raffetto ◽  
R A Khalil
Keyword(s):  
Varicose Vein ◽  
Structural Integrity ◽  
Cell Injury ◽  
Varicose Veins ◽  
Venous Pressure ◽  
Venous Disease ◽  
Vein Wall ◽  
Valve Dysfunction ◽  
Functional Changes ◽  
Vein Formation

Varicose veins are a common venous disease of the lower extremity. Although the mechanisms and determinants in the development of varicosities are not clearly defined, recent clinical studies and basic science research have cast some light on possible mechanisms of the disease. In varicose veins, there are reflux and incompetent valves as well as vein wall dilation. Primary structural changes in the valves may make them ‘leaky’, with progressive reflux causing secondary changes in the vein wall. Alternatively, or concurrently, the valves may become incompetent secondary to structural abnormalities and focal dilation in vein wall segments near the valve junctions, and the reflux ensues as an epiphenomenon. The increase in venous pressure causes structural and functional changes in the vein wall that leads to further venous dilation. Increase in vein wall tension augments the expression/activity of matrix metalloproteinases (MMPs), which induces degradation of the extracellular matrix proteins and affect the structural integrity of the vein wall. Recent evidence also suggests an effect of MMPs on the endothelium and smooth muscle components of the vein wall and thereby causing changes in the venous constriction/relaxation properties. Endothelial cell injury also triggers leukocyte infiltration, activation and inflammation, which lead to further vein wall damage. Thus, vein wall dilation appears to precede valve dysfunction, and the MMP activation and superimposed inflammation and fibrosis would then lead to chronic and progressive venous insufficiency and varicose vein formation.

Matrix metalloproteinases and tissue remodeling in hypertrophic cardiomyopathy

2008 ◽  
Vol 156 (1) ◽  
pp. 85-91 ◽  
Author(s):  
Vanessa Roldán ◽  
Francisco Marín ◽  
Juan R. Gimeno ◽  
Francisco Ruiz-Espejo ◽  
Josefa González ◽  
...  
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Matrix Metalloproteinases ◽  
Tissue Remodeling

scholarly journals Suprapubic varicose vein formation during pregnancy following pre-pregnancy pelvic vein embolisation with coils, without any residual pelvic venous reflux or obstruction

2017 ◽  
Vol 5 ◽  
pp. 2050313X1772471 ◽  
Author(s):  
Emma Dabbs ◽  
Jaya L Nemchand ◽  
Mark S Whiteley
Keyword(s):  
Varicose Vein ◽  
Varicose Veins ◽  
Iliac Vein ◽  
Subsequent Pregnancy ◽  
Common Iliac Vein ◽  
Venous Reflux ◽  
Foam Sclerotherapy ◽  
Pelvic Vein ◽  
Vein Formation ◽  
Collateral Vein

Suprapubic varicose veins are usually indicative of unilateral iliac vein occlusion and venous collateralisation. We report two cases of suprapubic varicose veins following pelvic vein embolisation and subsequent pregnancy; both presented without residual pelvic venous reflux or pelvic venous obstruction. In both cases, there was no significant flow in the suprapubic veins indicating that they were not acting as a collateral post-pregnancy. One patient had this venous abnormality treated successfully with TRansluminal Occlusion of Perforators, followed by foam sclerotherapy to the main part of the suprapubic vein. This patient has since completed the reminder of her lower limb varicose vein treatment. We suggest that pregnancy may have caused prolonged intermittent compression of the left common iliac vein, and that this, together with the physiological impact of previous embolisation procedures, obstructed venous drainage from the left leg resulting in collateral vein formation within the 9-month gestation period.

Ovarian tissue remodeling: role of matrix metalloproteinases and their inhibitors

2002 ◽  
Vol 191 (1) ◽  
pp. 45-56 ◽  
Author(s):  
Michael F. Smith ◽  
William A. Ricke ◽  
Leanne J. Bakke ◽  
Mark P.D. Dow ◽  
George W. Smith
Keyword(s):  
Matrix Metalloproteinases ◽  
Ovarian Tissue ◽  
Tissue Remodeling

scholarly journals Extracellular Matrix Degradation and Tissue Remodeling in Periprosthetic Loosening and Osteolysis: Focus on Matrix Metalloproteinases, Their Endogenous Tissue Inhibitors, and the Proteasome

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Spyros A. Syggelos ◽  
Alexios J. Aletras ◽  
Ioanna Smirlaki ◽  
Spyros S. Skandalis
Keyword(s):  
Extracellular Matrix ◽  
Matrix Metalloproteinases ◽  
Molecular Mechanisms ◽  
Total Joint Replacement ◽  
Proteolytic Enzymes ◽  
Tissue Remodeling ◽  
Wear Particle ◽  
Matrix Degradation ◽  
Tissue Inhibitors ◽  
Extracellular Matrix Degradation

The leading complication of total joint replacement is periprosthetic osteolysis, which often results in aseptic loosening of the implant, leading to revision surgery. Extracellular matrix degradation and connective tissue remodeling around implants have been considered as major biological events in the periprosthetic loosening. Critical mediators of wear particle-induced inflammatory osteolysis released by periprosthetic synovial cells (mainly macrophages) are inflammatory cytokines, chemokines, and proteolytic enzymes, mainly matrix metalloproteinases (MMPs). Numerous studies reveal a strong interdependence of MMP expression and activity with the molecular mechanisms that control the composition and turnover of periprosthetic matrices. MMPs can either actively modulate or be modulated by the molecular mechanisms that determine the debris-induced remodeling of the periprosthetic microenvironment. In the present study, the molecular mechanisms that control the composition, turnover, and activity of matrix macromolecules within the periprosthetic microenvironment exposed to wear debris are summarized and presented. Special emphasis is given to MMPs and their endogenous tissue inhibitors (TIMPs), as well as to the proteasome pathway, which appears to be an elegant molecular regulator of specific matrix macromolecules (including specific MMPs and TIMPs). Furthermore, strong rationale for potential clinical applications of the described molecular mechanisms to the treatment of periprosthetic loosening and osteolysis is provided.

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