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Anthracycline-dependent cardiotoxicity and extracellular matrix remodeling.
Journal article

Anthracycline-dependent cardiotoxicity and extracellular matrix remodeling.

  • Nikitovic D Department of Anatomy-Histology-Embryology, School of Medicine, University of Crete, Heraklion, Greece. Electronic address: dnikitovic@med.uoc.gr.
  • Juranek I Institute of Experimental Pharmacology and Toxicology, Slovak Academy of Sciences, Bratislava, Slovakia.
  • Wilks MF Swiss Centre for Applied Human Toxicology, University of Basel, Basel, Switzerland.
  • Tzardi M Department of Pathology, School of Medicine, University of Crete, Heraklion, Greece.
  • Tsatsakis A Department of Forensic Sciences and Toxicology, School of Medicine, University of Crete, Heraklion, Greece.
  • Tzanakakis GN Department of Anatomy-Histology-Embryology, School of Medicine, University of Crete, Heraklion, Greece.
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  • 2014-10-08
Published in:
  • Chest. - 2014
Anthracyclines
Antibiotics, Antineoplastic
Cardiotoxicity
Extracellular Matrix
Heart
Humans
Ventricular Remodeling
English The mechanisms of anthracycline-dependent cardiotoxicity have been studied widely, with the suggested principal mechanism of anthracycline damage being the generation of reactive oxygen species by iron-anthracycline complexes, leading to lipid peroxidation and membrane damage. An increasing number of researchers studying cardiovascular events associated with anthracycline-based chemotherapy are addressing cardiac extracellular matrix (ECM) remodeling. The heart is an efficient muscular pump, with the cardiomyocytes and intramural coronary vasculature of the heart tethered in an ECM consisting of a network of fibrillar, structural proteins, mostly collagens. Increasing evidence suggests that the ECM plays a complex and diverse role in the processes initiated by anthracycline-class drugs that lead to cardiac damage. This review discusses adverse myocardial remodeling induced by anthracyclines and focuses on their mechanisms of action.
Language
  • English
Open access status
closed
Identifiers
Persistent URL
https://sonar.ch/global/documents/53427
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