Associations between collagen synthesis and degradation and aortic function in arterial hypertension

Dimitrios A Stakos1, Dimitrios N Tziakas, George K Chalikias

  • 1Department of Cardiology, Medical School, Democritus University of Thrace, Alexandroupolis, Greece. dstakos@med.duth.gr

Insights

Hypertension is linked to increased aortic stiffness due to collagen changes. This study found that altered collagen type I synthesis and proMMP-1 expression correlate with stiffer aortas in hypertensive patients.

Area of Science:

  • Cardiovascular Research
  • Biochemistry
  • Hypertension Research

Background:

  • Aortic stiffness is a hallmark of arterial hypertension.
  • Collagen accumulation in the aorta is a potential contributor to this stiffness.
  • Human data on collagen metabolism and aortic function in hypertension are limited.

Purpose of the Study:

  • To investigate the relationship between collagen metabolism markers and aortic stiffness in hypertensive patients.
  • To evaluate collagen type I and III synthesis and degradation markers.
  • To assess matrix metalloproteinase-1 (MMP-1) and its inhibitor (TIMP-1) in relation to aortic function.

Main Methods:

  • Cross-sectional study of 72 hypertensive patients and 27 normotensive controls.
  • Aortic stiffness assessed using carotid-to-femoral pulse wave velocity (PWVc-f).
  • Serum levels of collagen synthesis (PINP) and degradation (CITP) markers, collagen III metabolism (PIIINP), proMMP-1, and TIMP-1 were measured.

Main Results:

  • Hypertensive patients exhibited greater PWVc-f and higher levels of collagen type I synthesis and degradation markers (PINP/CITP).
  • PWVc-f was significantly associated with the PINP/CITP ratio.
  • Increased proMMP-1 and proMMP-1/TIMP-1 levels were observed in hypertensive patients, correlating with PWVc-f.

Conclusions:

  • Altered collagen turnover favoring collagen type I synthesis is linked to increased aortic stiffness in hypertensive individuals.
  • Elevated proMMP-1 expression is also associated with increased aortic stiffness.
  • These findings hold true even in treated hypertensive patients without left ventricular hypertrophy.
Abstract

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