Collagen network of the myocardium

Function, structural remodeling and regulatory mechanisms

Karl Weber, Yao Sun, Suresh C. Tyagi, Jack P.M. Cleutjens

Research output: Contribution to journalReview article

396 Citations (Scopus)

Abstract

A collagen network, composed largely of type I and III fibrillar collagens, is found in the extracellular space of the myocardium. This network has multiple functions which includes a preservation of tissue architecture and chamber geometry. Given its tensile strength, collagen is a major determinant of tissue stiffness. Its disproportionate accumulation, in the form of either a reactive or a reparative fibrosis, further increases stiffness. A degradation of collagen tethers, on the other hand, is an anatomic requisite for a distortion in tissue architecture and a reduction in stiffness that can lead to chamber dilatation, wall thinning, and even rupture of the myocardium. Collagen turnover in the myocardium is dynamic. When synthesis exceeds degradation, an adverse accumulation of collagen appears to distort tissue structure. This is true for either the hypertrophied and/or nonhypertrophied ventricle. Factors that contribute to the appearance of myocardial fibrosis are largely different from those that promote cardiac myocyte growth. Included amongst these fibrogenic factors are effector hormones of the reinin-angiotensin-aldosterone system (RAAS). Studies conducted both in intact animals (relative to dietary sodium intake) and in cultured adult cardiac fibroblasts have pointed toward the association between collagen accumulation and chronic elevations in circulating angiotensin II and aldosterone. A tissue hormonal system involving angiotensin II, endothelins and bradykinin, may likewise regulate fibrogenesis. In this regard, angiotensin converting enzyme is found in connective tissue of the normal heart, including the matrix of heart valves and the adventitia of the intramural coronary arteries, and fibrous tissue that forms following infarction or with chronic RAAS activation. The importance of ACE in the regulation of local angiotensin II and bradykinin levels and their contribution to collagen turnover is a fruitful area of research with important clinical implications. The myocardium also contains a proteolytic system, including collagenase. The characteristics and regulation of matrix metalloproteinases and their tissue inhibitors in various cardiovascular disease states requires further investigation.

Original languageEnglish (US)
Pages (from-to)279-292
Number of pages14
JournalJournal of Molecular and Cellular Cardiology
Volume26
Issue number3
DOIs
StatePublished - Jan 1 1994

Fingerprint

Myocardium
Collagen
Aldosterone
Angiotensin II
Angiotensins
Bradykinin
Fibrosis
Fibrillar Collagens
Tissue Preservation
Dietary Sodium
Adventitia
Tensile Strength
Endothelins
Heart Valves
Extracellular Space
Collagenases
Peptidyl-Dipeptidase A
Matrix Metalloproteinases
Cardiac Myocytes
Connective Tissue

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine

Cite this

Collagen network of the myocardium : Function, structural remodeling and regulatory mechanisms. / Weber, Karl; Sun, Yao; Tyagi, Suresh C.; Cleutjens, Jack P.M.

In: Journal of Molecular and Cellular Cardiology, Vol. 26, No. 3, 01.01.1994, p. 279-292.

Research output: Contribution to journalReview article

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