Proteomic and Metabolomic Profiles in Atherothrombotic Vascular Disease Roxana Martinez-Pinna & Coral Barbas & Luis Miguel Blanco-Colio & Jose Tunon & Priscila Ramos-Mozo & Juan Antonio Lopez & Olivier Meilhac & Jean-Baptiste Michel & Jesus Egido & José Luis Martin-Ventura Published online: 23 March 2010 # Springer Science+Business Media, LLC 2010 Abstract Atherothrombosis remains a major cause of morbidity and mortality in the western world. The underlying processes associated with clinical expression of atherothrombosis include oxidative stress and proteolysis in relation to neovascularisation and intraplaque hemorrhages, leading to immuno-inflammatory response, cell death, and extracellular matrix breakdown. The complex biological multifactorial nature of atherothrombosis requires the development of novel technologies that allow the analysis of cellular and molecular processes responsible for the transition to disease phenotypes and the discovery of new diagnostic and prognostic biomarkers. In the present article, we have reviewed recent advances in the application of proteomic and metabolomic techniques to the study of atherothrombosis. We have focused on recent studies analyzing cells involved in hemo-thrombus formation (platelets, red blood cells, and polymorphonuclear cells), as well as tissues, tissue-conditioned media, and plasma of atherothrombotic patients. In the future, the application of these high-throughput technologies, along with imaging techniques, in systems biology approaches will help to individualize medicine. Keywords Proteomics . Metabolomics . Biomarkers . Atherosclerosis . Abdominal aortic aneurysm Introduction Atherothrombosis remains a major cause of morbidity and mortality in the western world, whether the localization is related to coronary/carotid/peripheral artery disease or aneurysms of the abdominal aorta (AAA) [1–3]. The complex biological processes associated with atherothrom- bosis include oxidative stress and proteolysis in relation to neovascularization and intraplaque hemorrhages, leading to immuno-inflammatory response, cell death, and extracellu- lar matrix breakdown. Intraplaque hemorrhage is a main mechanism in atherothrombosis [4–7], linking biology to clinical expression of the disease. In this respect, recent studies suggest that neoangiogenesis is the primary source of intraplaque hemorrhage at sites of microvessel incom- petence [8], with leakage of red blood cells (RBCs) into the plaque, which induces cycles of oxidative stress, leukocyte recruitment, and neovascularization. Similarly, intraluminal thrombus (ILT) is involved in the evolution of AAA, R. Martinez-Pinna : L. M. Blanco-Colio : P. Ramos-Mozo : J. Egido : J. L. Martin-Ventura (*) Vascular Research Laboratory, Instituto de Investigacion Sanitaria, Fundación Jimenez Diaz, Autonoma University, Av. Reyes Católicos 2, 28040 Madrid, Spain e-mail: jlmartin@fjd.es C. Barbas Pharmacy Faculty, Campus Monteprincipe, San Pablo-CEU University, 28668 Boadilla del Monte, Madrid, Spain J. Tunon Department of Cardiology, Instituto de Investigaciones Sanitarias, Fundación Jimenez Diaz, Autonoma University, Av. Reyes Católicos 2, 28040 Madrid, Spain J. A. Lopez Unidad de Proteomica, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain O. Meilhac : J.-B. Michel Inserm, U698, Univ Paris 7, CHU X-Bichat, Paris, France Curr Atheroscler Rep (2010) 12:202–208 DOI 10.1007/s11883-010-0102-y