Reprint of "The complex dynamics of myocardial interstitial fibrosis in heart failure. Focus on collagen cross-linking"
González A (1), López B (2), Ravassa S (2), San José G (2), Díez J (3)
(1) Program of Cardiovascular Diseases, CIMA Universidad de Navarra and IdiSNA, Pamplona, Spain; CIBERCV, Carlos III Institute of Health, Madrid, Spain.
(2) Program of Cardiovascular Diseases, CIMA Universidad de Navarra and IdiSNA, Pamplona, Spain; CIBERCV, Carlos III Institute of Health, Madrid, Spain.
(3) Program of Cardiovascular Diseases, CIMA Universidad de Navarra and IdiSNA, Pamplona, Spain; CIBERCV, Carlos III Institute of Health, Madrid, Spain; Departments of Cardiology and Cardiac Surgery and of Nephrology, Clínica Universidad de Navarra, Pamplona, Spain.
Revisão:Biochimica and Biophysical Acta. Molecular Cell Research
Data: 5/Ago/2019Nefrologia [ES]
Myocardial interstitial fibrosis (MIF) is a common finding in heart failure (HF) patients, both with preserved and reduced ejection fraction, as well as in HF animal models. MIF is associated with impaired cardiac function and worse clinical outcome.
The impact of MIF is influenced not only by the quantity but also by changes in the quality of collagen fibers and in the extracellular matrix components, such as a shift in collagen types proportion, increased fibronectin polymerization and increased degree of collagen cross-linking (CCL).
In particular, CCL, a process that renders collagen fibers stiffer and more resistant to degradation, is increased both in patients and animal models of HF. Importantly, in HF patients increased cardiac CCL is directly associated with increased left ventricular stiffness and a higher risk of hospitalization for HF.
The aim of this review is to address the complexity of MIF in HF, focusing on CCL.
CITAÇÃO DO ARTIGO Biochim Biophys Acta Mol Cell Res. 2019 Aug 5. pii: S0167-4889(19)30129-6. doi: 10.1016/j.bbamcr.2019.07.016
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