Genetics of inflammation in age-related atherosclerosis: its relevance to pharmacogenomics.

Abstract

In response to tissue injury elicited by trauma or infection, the inflammatory response, as a complex network of molecular and cellular interactions, sets an answer directed to facilitate a return to physiological homeostasis and tissue repair. The role of the genetic background and the subsequent predisposition toward the extent of the inflammatory response is determined by gene variability encoding endogenous mediators involved in the inflammatory pathway. Due to its clinical relevance, the genetics of inflammation in aging will be studied using an inflammatory disease like atherosclerosis as an example. Several studies have reported a significant difference in distribution, between patients and controls, of genes involved in inflammation. So, the proinflammatory alleles are underrepresented in control subjects and overrepresented in patients affected by atherosclerosis. These studies will allow building a risk profile that potentially enables the early identification of individuals susceptible to disease and the possible design or use of drug at the right dose for a desired effect, that is, a pharmacogenomic approach for this disease.