Smoking Clinical Trial - Endostatin Serum Levels During Bicycle Stress

Status Completed

Clinical Trial Summary

Endostatin, a 20-kDa cleavage product of collagen XVIII, is a component of the extracellular matrix expressed in the basement membrane. As a potent inhibitor of angiogenesis, endostatin induces endothelial cell apoptosis and diminishes cell migration, adhesion and proliferation.

Endostatin may stop the progression of atherosclerosis. Atherosclerotic heart disease involves unwanted tissue growth. By cutting off the blood supply from a plaque the likelihood of plaque rupture may eventually be reduced. Recent data indicates that the loss of collagen XVIII/endostatin is related to the enhancement of neo-vascularization and vascular permeability in atherosclerosis. Plaque neo-vascularization strongly correlates with the regional content of inflammatory cells. Furthermore, increased vascular permeability enhances lipid accumulation in the vessel walls, hence increasing foam cells.

Therapeutic angiogenesis is a most promising strategy for the treatment of myocardial infarction. However, it remains unknown if and how endogenous angiogenesis inhibitors, such as endostatin, regulate angiogenesis in myocardial infarction. Rat models showed that after myocardial infarction endostatin neutralization displayed adverse left ventricular remodeling and severe heart failure compared with controls. Although angiogenesis was increased, tissue remodeling and interstitial fibrosis were further exaggerated in post-myocardial infarction hearts by endostatin neutralization.

However, several studies suggest that endostatin may locally modulate coronary collateral formation by inhibiting collateral vessel formation in patients with ischemic heart disease.

During treadmill exercise tests in healthy volunteers a significant increase in circulating endostatin levels can be observed. Exercise induces angiogenesis in cardiac and skeletal muscles by decreasing endostatin in the muscle tissues to increase blood flow to these metabolically active tissues. Thereby endostatin is released into the general circulation.

In summary, endostatin might be a new weapon to fight against atherosclerotic progression by inhibiting neo-vascularization of atherosclerotic plaques.

Clinical Trial Description

n/a

Study Design

Time Perspective: Prospective

Related Conditions & MeSH terms

Clinical Trial Details

NCT number	NCT01165515
Study type	Observational
Source	Medical University of Vienna
Contact
Status	Completed
Phase	N/A
Start date	January 2008
Completion date	April 2013

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Clinical trials are conducted in a series of steps, called phases - each phase is designed to answer a separate research question.

Phase 1: Researchers test a new drug or treatment in a small group of people for the first time to evaluate its safety, determine a safe dosage range, and identify side effects.
Phase 2: The drug or treatment is given to a larger group of people to see if it is effective and to further evaluate its safety.
Phase 3: The drug or treatment is given to large groups of people to confirm its effectiveness, monitor side effects, compare it to commonly used treatments, and collect information that will allow the drug or treatment to be used safely.
Phase 4: Studies are done after the drug or treatment has been marketed to gather information on the drug's effect in various populations and any side effects associated with long-term use.

Endostatin Serum Levels During Bicycle Stress Test

Clinical Trial Summary

Clinical Trial Description

Study Design

Related Conditions & MeSH terms