Biochemistry Insights 2011:4 13-27
Published on 11 May 2011
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Cardiovascular disease, commonly manifested as myocardial infarction (MI), is a significant health problem worldwide that in the United States, accounts for one out of every three deaths and remains a significant health problem. Notwithstanding the concerted treatment efforts to target the major pathomechanisms and protect MI patients from ongoing vascular pathology, inflammatory processes have been noted in these cohorts. Results from this multiethnic cohort study by Dr. Szauter and colleagues identified coordinated upregulation of genes for inflammation, T-cell activation, and atherosclerosis and demonstrated that multiple inflammatory pathways, undetected by standard laboratory tests, persist together with immune imbalance and active atherogenesis in medicated MI patients. Data in this Hawaii study population indicated ethnic-specific differences in active inflammatory pathways and highlighted the need for additional ethnicity-based studies to determine specific pathology profiles in particular patient populations for improved treatment modalities that target pathomechanisms unresponsive to current therapies.
In spite of current standard therapies to target the major pathomechanisms in myocardial infarction (MI), inflammatory gene expression patterns have been consistently revealed in MI patients. In a multiethnic cohort, we aimed to identify MI-associated pathomechanisms that may be unresponsive to medical treatment to improve diagnosis and therapy. Gene expression profiles in whole blood were analyzed in medicated Asian, African American and Caucasian patients living in Hawaii with a history of early MI and age, ethnicity, risk factor and medication-matched controls. PANTHER ontological and Ingenuity Pathway analysis and functional evaluation of the consistently differentially expressed genes identified coordinated up-regulation of genes for inflammation (LGALS3, PTX3, ZBTB32, BCL2L1), T-cell activation (IL12RB1, VAV3, JAG1, CAMP), immune imbalance (IL-8, IL2RA, CCR7, AHNAK), and active atherosclerosis (NR1H4, BIN1, GSTT1, MARCO) that persist in MI patients in spite of concerted treatment efforts to control vascular pathology. Furthermore, significant ethnic differences appear to exist within the active disease mechanisms that need to be further investigated to identify key targets for effective medical intervention.
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