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- W1999717948 abstract "Several distinct stimuli can be used to reproduce histological and functional features of human emphysema, a leading cause of disability and death. Since cigarette smoke is the main cause of emphysema in humans, experimental researches have attempted to reproduce this situation. However, this is an expensive and cumbersome method of emphysema induction, and simpler, more efficacious alternatives have been sought. Among these approaches, elastolytic enzymes have been widely used to reproduce some characteristics of human cigarette smoke-induced disease, such as: augmentation of airspaces, inflammatory cell influx into the lungs, and systemic inflammation. Nevertheless, the use of elastase-induced emphysema models is still controversial, since the disease pathways involved in elastase induction may differ from those occurring in smoke-induced emphysema. This indicates that the choice of an emphysema model may impact the results of new therapies or drugs being tested. The aim of this review is to compare the mechanisms of disease induction in smoke and elastase emphysema models, to describe the differences among various elastase models, and to establish the advantages and disadvantages of elastase-induced emphysema models. More studies are required to shed light on the mechanisms of elastase-induced emphysema." @default.
- W1999717948 created "2016-06-24" @default.
- W1999717948 creator A5085125003 @default.
- W1999717948 creator A5091455922 @default.
- W1999717948 date "2011-10-07" @default.
- W1999717948 modified "2023-09-30" @default.
- W1999717948 title "Elastase-induced pulmonary emphysema: insights from experimental models" @default.
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- W1999717948 doi "https://doi.org/10.1590/s0001-37652011005000039" @default.
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