The pathobiological mechanisms of emphysema models: What do they have in common?

Tuder, Rubin M.; McGrath, Sharon; Neptune, Enid

doi:10.1016/s1094-5539(02)00099-8

Cited by 67 publications

(54 citation statements)

References 71 publications

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“…HIV-infected persons might have increased susceptibility to apoptosis because the HIV proteins Tat and Nef may induce endothelial cell apoptosis (49). It is also possible that HIV may cause apoptosis directly (50,51).…”

Section: Apoptosismentioning

confidence: 99%

HIV and Chronic Obstructive Pulmonary Disease: Is It Worse and Why?

Morris¹,

George²,

Crothers³

et al. 2011

Proceedings of the American Thoracic Society

109

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Section: Apoptosismentioning

confidence: 99%

HIV and Chronic Obstructive Pulmonary Disease: Is It Worse and Why?

Morris¹,

George²,

Crothers³

et al. 2011

Proceedings of the American Thoracic Society

109

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“…A delicate balance between protease and antiprotease activity is required for proper lung maintenance (1). Derangements of this balance may result in increased destruction and inappropriate repair of lungs, ultimately causing emphysema.…”

Section: Protease-antiprotease Balancementioning

confidence: 99%

Pathogenesis of Emphysema: From the Bench to the Bedside

Sharafkhaneh¹,

Hanania²,

Kim³

2008

Proceedings of the American Thoracic Society

173

119

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Chronic obstructive pulmonary disease (COPD) is characterized physiologically by expiratory flow limitation and pathologically by alveolar destruction and enlargement and small and large airway inflammation and remodeling. An imbalance between protease and antiprotease activity in the lung is proposed as the major mechanism resulting in emphysema. The imbalance is mostly due to an increase in the numbers of alveolar macrophages and neutrophils. Emphysema can also develop from increased alveolar wall cell death and/or failure in alveolar wall maintenance. Chronic inflammation and increased oxidative stress contribute to increased destruction and/ or impaired lung maintenance and repair. Genetic factors may play an important role in disease susceptibility because only a minority of smokers develops emphysema. Recent literature implicates surfactant instability, malnutrition, and alveolar cell apoptosis as possible etiologies. Identification of cellular and molecular mechanisms of COPD pathogenesis is an area of active, ongoing research that may help to determine therapeutic targets for emphysema.

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“…Among these mechanisms, protease-antiprotease imbalance, oxidative stress, inflammation, apoptosis and matrix remodelling are on top of the list [10]. Yet, it is striking that even if the original causes are removed, the disease still progresses and leads to severe destruction of the lung and, eventually, respiratory insufficiency.…”

mentioning

confidence: 99%