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.
Lingua originaleEnglish
pagine (da-a)123-131
Numero di pagine9
RivistaAnnals of the New York Academy of Sciences
Volume1100
Stato di pubblicazionePublished - 2007

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Pharmacogenetics
Atherosclerosis
Inflammation
Tissue
Gene encoding
Wounds and Injuries
Complex networks
Genes
Homeostasis
Repair
Aging of materials
Alleles
Infection
Pharmaceutical Preparations
Genetics
Pharmacogenomics
Gene

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • History and Philosophy of Science
  • Biochemistry, Genetics and Molecular Biology(all)

Cita questo

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title = "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.",
author = "Calogero Caruso and Giuseppina Candore and Domenico Lio and Egle Incalcaterra and {Di Carlo}, Daniele and Balistreri, {Carmela Rita} and Sonya Vasto and Grimaldi, {Maria Paola} and Giuseppina Candore",
year = "2007",
language = "English",
volume = "1100",
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journal = "Annals of the New York Academy of Sciences",
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TY - JOUR

T1 - Genetics of inflammation in age-related atherosclerosis: its relevance to pharmacogenomics.

AU - Caruso, Calogero

AU - Candore, Giuseppina

AU - Lio, Domenico

AU - Incalcaterra, Egle

AU - Di Carlo, Daniele

AU - Balistreri, Carmela Rita

AU - Vasto, Sonya

AU - Grimaldi, Maria Paola

AU - Candore, Giuseppina

PY - 2007

Y1 - 2007

N2 - 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.

AB - 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.

UR - http://hdl.handle.net/10447/9213

M3 - Article

VL - 1100

SP - 123

EP - 131

JO - Annals of the New York Academy of Sciences

JF - Annals of the New York Academy of Sciences

SN - 0077-8923

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