Genomic investigations into acute inflammatory lung injury

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome, are complex illnesses involving the interplay of both environmental (such as mechanical ventilation) and genetic factors. To understand better the underlying mechanisms of pathogenesis associated with ALI, we recently identified several candidate genes by global expression profiling in preclinical models of ALI and relevant single-nucleotide polymorphisms. We summarize here several strategies successfully used to identify novel ALI candidate genes and detail the validation of variants in these genes as contributing factors to ALI pathobiology, conclusions based on functional analyses, and specific genetic association studies conducted in ALI cohorts. Continued insights into ALI pathogenesis and identification of genetic variants, which confer ALI risk and severity, promise to reveal novel molecular therapeutic targets that can be translated into personalized treatments to reduce the very high, unacceptable mortality of this disorder.

Original languageEnglish (US)
Pages (from-to)167-172
Number of pages6
JournalProceedings of the American Thoracic Society
Volume8
Issue number2
DOIs
StatePublished - May 1 2011
Externally publishedYes

Fingerprint

Acute Lung Injury
Adult Respiratory Distress Syndrome
Genetic Association Studies
Gene Expression Profiling
Artificial Respiration
Genes
Single Nucleotide Polymorphism
Mortality
Therapeutics

Keywords

  • Acute lung injury
  • Inflammation
  • Microarray
  • PBEF
  • SNP

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Genomic investigations into acute inflammatory lung injury. / Garcia, Joe GN.

In: Proceedings of the American Thoracic Society, Vol. 8, No. 2, 01.05.2011, p. 167-172.

Research output: Contribution to journalArticle

@article{0319b6cec33f49f68e259876df75a884,
title = "Genomic investigations into acute inflammatory lung injury",
abstract = "Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome, are complex illnesses involving the interplay of both environmental (such as mechanical ventilation) and genetic factors. To understand better the underlying mechanisms of pathogenesis associated with ALI, we recently identified several candidate genes by global expression profiling in preclinical models of ALI and relevant single-nucleotide polymorphisms. We summarize here several strategies successfully used to identify novel ALI candidate genes and detail the validation of variants in these genes as contributing factors to ALI pathobiology, conclusions based on functional analyses, and specific genetic association studies conducted in ALI cohorts. Continued insights into ALI pathogenesis and identification of genetic variants, which confer ALI risk and severity, promise to reveal novel molecular therapeutic targets that can be translated into personalized treatments to reduce the very high, unacceptable mortality of this disorder.",
keywords = "Acute lung injury, Inflammation, Microarray, PBEF, SNP",
author = "Garcia, {Joe GN}",
year = "2011",
month = "5",
day = "1",
doi = "10.1513/pats.201101-002MS",
language = "English (US)",
volume = "8",
pages = "167--172",
journal = "Annals of the American Thoracic Society",
issn = "2325-6621",
publisher = "American Thoracic Society",
number = "2",

}

TY - JOUR

T1 - Genomic investigations into acute inflammatory lung injury

AU - Garcia, Joe GN

PY - 2011/5/1

Y1 - 2011/5/1

N2 - Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome, are complex illnesses involving the interplay of both environmental (such as mechanical ventilation) and genetic factors. To understand better the underlying mechanisms of pathogenesis associated with ALI, we recently identified several candidate genes by global expression profiling in preclinical models of ALI and relevant single-nucleotide polymorphisms. We summarize here several strategies successfully used to identify novel ALI candidate genes and detail the validation of variants in these genes as contributing factors to ALI pathobiology, conclusions based on functional analyses, and specific genetic association studies conducted in ALI cohorts. Continued insights into ALI pathogenesis and identification of genetic variants, which confer ALI risk and severity, promise to reveal novel molecular therapeutic targets that can be translated into personalized treatments to reduce the very high, unacceptable mortality of this disorder.

AB - Acute lung injury (ALI) and its more severe form, acute respiratory distress syndrome, are complex illnesses involving the interplay of both environmental (such as mechanical ventilation) and genetic factors. To understand better the underlying mechanisms of pathogenesis associated with ALI, we recently identified several candidate genes by global expression profiling in preclinical models of ALI and relevant single-nucleotide polymorphisms. We summarize here several strategies successfully used to identify novel ALI candidate genes and detail the validation of variants in these genes as contributing factors to ALI pathobiology, conclusions based on functional analyses, and specific genetic association studies conducted in ALI cohorts. Continued insights into ALI pathogenesis and identification of genetic variants, which confer ALI risk and severity, promise to reveal novel molecular therapeutic targets that can be translated into personalized treatments to reduce the very high, unacceptable mortality of this disorder.

KW - Acute lung injury

KW - Inflammation

KW - Microarray

KW - PBEF

KW - SNP

UR - http://www.scopus.com/inward/record.url?scp=80051715542&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=80051715542&partnerID=8YFLogxK

U2 - 10.1513/pats.201101-002MS

DO - 10.1513/pats.201101-002MS

M3 - Article

C2 - 21543796

AN - SCOPUS:80051715542

VL - 8

SP - 167

EP - 172

JO - Annals of the American Thoracic Society

JF - Annals of the American Thoracic Society

SN - 2325-6621

IS - 2

ER -