Molecular Imaging of the Cardiac Extracellular Matrix

Autor: Christopher M. Kramer, Valentin Fuster, Jagat Narula, Eloisa Arbustini, Hans J. de Haas
Jazyk: angličtina
Rok vydání: 2014
Předmět:
ANGIOTENSIN-CONVERTING ENZYME
Pathology
medicine.medical_specialty
Heart disease
Heart Diseases
Physiology
heart failure
HEART-DISEASE
030204 cardiovascular system & hematology
Matrix metalloproteinase
ACTIVITY IN-VIVO
030218 nuclear medicine & medical imaging
Extracellular matrix
03 medical and health sciences
0302 clinical medicine
TENASCIN-C
Fibrosis
METALLOPROTEINASE ACTIVITY
Medicine
Animals
Humans
Myocardial infarction
Myofibroblasts
Extracellular Matrix Proteins
biology
business.industry
Tenascin C
ALPHA(V)BETA(3) INTEGRIN EXPRESSION
molecular imaging
medicine.disease
PRELIMINARY BIOLOGICAL EVALUATION
Extracellular Matrix
Cardiac Imaging Techniques
CARDIOVASCULAR MAGNETIC-RESONANCE
Heart failure
biology.protein
DIFFUSE MYOCARDIAL FIBROSIS
CONTRAST AGENT P947
Cardiology and Cardiovascular Medicine
business
Myofibroblast
Zdroj: Circulation Research; Vol 114
Circulation Research
ISSN: 0009-7330
DOI: 10.1161/CIRCRESAHA.113.302680
Popis: In almost all cardiac diseases, an increase in extracellular matrix (ECM) deposition or fibrosis occurs, mostly consisting of collagen I. Whereas replacement fibrosis follows cardiomyocyte loss in myocardial infarction, reactive fibrosis is triggered by myocardial stress or inflammatory mediators and often results in ventricular stiffening, functional deterioration, and development of heart failure. Given the importance of ECM deposition in cardiac disease, ECM imaging could be a valuable clinical tool. Molecular imaging of ECM may help understand pathology, evaluate impact of novel therapy, and may eventually find a role in predicting the extent of ECM expansion and development of personalized treatment. In the current review, we provide an overview of ECM imaging including the assessment of ECM volume and molecular targeting of key players involved in ECM deposition and degradation. The targets comprise myofibroblasts, intracardiac renin-angiotensin axis, matrix metalloproteinases, and matricellular proteins.
Databáze: OpenAIRE
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