IBIMOL   23987
INSTITUTO DE BIOQUIMICA Y MEDICINA MOLECULAR PROFESOR ALBERTO BOVERIS
Unidad Ejecutora - UE
artículos
Título:
Metalloproteinase 2 and 9 Activity Increase in Epicardial Adipose Tissue of Patients with Coronary Artery Disease
Autor/es:
MIKSZTOWICZ V; MORALES C; BARCHUK M; LÓPEZ GI; PÓVEDA R; GELPI R; SCHREIER L; RUBIO M; BERG G; MIKSZTOWICZ V; MORALES C; BARCHUK M; LÓPEZ GI; PÓVEDA R; GELPI R; SCHREIER L; RUBIO M; BERG G
Revista:
CURRENT VASCULAR PHARMACOLOGY
Editorial:
BENTHAM SCIENCE PUBL LTD
Referencias:
Lugar: Oak Park; Año: 2017 vol. 15 p. 135 - 143
ISSN:
1570-1611
Resumen:
Background: Epicardial adipose tissue (EAT) is a visceral adipose tissue (AT) surrounding and infiltrating myocardium and coronary arteries. Increased EAT may represent a chronic inflammatory injury and a link with coronary artery disease (CAD). Metalloproteinases (MMPs) are involved in expansion of AT. Objective: to evaluate MMP-2 and -9 behaviour in EAT from CAD patients. Methods: In EAT and subcutaneous AT (SAT) from patients undergoing coronary artery bypass graft (CABG, n=26) or valve replacement (No CABG, n=18), MMP-2 and -9 activity and localization, inflammatory cells and vascular endothelial growth factor (VEGF) levels were determined. Results: In EAT from CABG, MMP-2 and -9 activity was increased compared with No CABG (p=0.041 and p=0.027, respectively) and compared with SAT (p=0.005 and p=0.048, respectively). In CABG patients EAT showed higher infiltration of macrophages and T lymphocytes than SAT (p=0.01 and p=0.002, respectively). In No CABG patients no sign of cellular retention was observed in EAT or SAT. Vascular density was higher in EAT from CABG than No CABG (p=0.015) and it was directly correlated with MMP-2 (p=0.006) and MMP-9 (p=0.02). VEGF levels in EAT were directly associated with MMP-2 (p=0.016). Conclusion: In EAT from CABG patients the increase of MMP-2 and -9 activity and the presence of inflammatory cells would be partially responsible of ECM remodeling and major vascular density necessary for EAT expansion. Improved knowledge of EAT behaviour may allow identify new therapeutic targets for the treatment of CAD.