Chronic obstructive pulmonary disease (COPD): a review from the literature of the different multi-model combination systems used to study a specific aspect of COPD pathogenesis

Area of researchMain focusMain experimental toolsReferences
Genetic factorsAlpha-1-antitrypsinCigarette smoke exposure of different mouse strains, gene deletion and transgenic overexpression[S327–S330]
GWAS loci associated with COPDCigarette smoke exposure, gene deficient mice, in vitro experimentation[S331–S334]
Lung developmentLung growthGene deficient animal models[S331, S335–S343]
Maternal smoking during pregnancyCigarette smoke exposure[S344–S347]
AgeingCigarette smoke exposure[S348, S349]
Environmental factorsTobacco smoke exposureCigarette smoke exposure[S350–S358]
In vitro systems[S350, S359]
Biomass fuelWood burning smoke exposure[S360]
Exposure to wood or cow dung particulate matter[S361]
Outdoor pollutionExposure to air pollutants[S351, S362–S364]
Microbial agentsLPS administration[S365–S370]
Airway remodellingAirway and vascular remodellingCigarette smoke exposure[S371, S372]
Alveolar destruction/emphysemaAirspace enlargementTransgenic mouse strains[S371, S373, S374]
Instillation of elastases[S353, S374, S375]
ExacerbationsBacteria-predominantCigarette smoke and bacterial agents[S376–S381]
Viral-predominantCigarette smoke and viral agents[S295, S382–S389]
ComorbiditiesCachexia/skeletal muscle wasting, cardiovascular[S353, S390–S395]

GWAS: genome-wide association study; LPS: lipopolysaccharide. For references listed in the table please refer to the supplementary material.