Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Integrins are the principle mediators of molecular dialog between a cell and its extracellular matrix environment. The unique combinations of integrin subunits determine which extracellular matrix molecules are recognized by a cell. Recent studies have demonstrated that remodeling in heart and vasculature is linked to alterations in extracellular matrix and integrin expression. The roles of integrins in controlling cellular behavior have made these molecules highly attractive drug targets. New insights into mechanisms whereby the extracellular matrix takes part in the control of smooth muscle cell proliferation and cardiac growth suggest a number of putative targets for future therapies that can be applied to increase plaque stability, prevent the clinical consequences of atherosclerosis and improve outcomes after interventional procedures such as cardiac transplantation. Therapeutic candidates include antibodies, cyclic peptides, peptidomimetics and small molecules. The integrin inhibitors Integrilin and ReoPro have been approved as blood thinners in cardiovascular disease, and newer agents are undergoing testing. Although integrin function is important in the cardiovascular system, there are wide gaps in knowledge. In this review, we discuss the primary mechanisms of action and signaling of integrins in the cardiac and vascular system in normal and pathological states, as well as therapeutic strategies for targeting these molecules in the cardiovascular system.
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PMID:Integrins: novel therapeutic targets for cardiovascular diseases. 1743 Jan 35

Inflammatory bowel diseases have been recognized as predisposing factors to atherosclerosis and thrombotic events, involving both the venous and the arterial circulatory systems. We report the case of a 70-year-old man who presented with ST elevation myocardial infarction during the active phase of ulcerative colitis (UC). Because of the ongoing hematochezia, after successful revascularization of the culprit vessel, the patient was medicated with Clopidogrel, in place of one of the more powerful new oral P2Y12 inhibitors that currently represent the gold standard therapy. Few days later a second elective percutaneous coronary intervention (PCI) on a non-culprit vessel ensued in a life-threatening early massive stent thrombosis involving the left main. During and after emergency PCI antiplatelet therapy was upgraded to Abciximab and Ticagrelor; this therapy proved successful in handling the massive stent thrombosis in the absence of severe bleeding complications. This case is unique and paradigmatic of the complex management of patients with coexisting active UC and acute coronary syndromes; it demonstrates as in this setting the balance between hemorrhagic and ischemic risk is labile and tricky to assess.
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PMID:Massive stent thrombosis during active ulcerative colitis: the tricky balance between manifest hemorrhagic and concealed thrombotic risk. 3013 27