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Current opinion in pharmacology  2008;8(3):255-260.
The discovery of vascular endothelial growth factor (VEGF) changed the field of angiogenesis. We have learned that VEGF has broader actions than merely a driver of tumor angiogenesis, particularly that VEGF controlled several fundamental functions and properties of endothelial cells and non-endothelial cells. The lung is one of the main organs where VEGF controls several critical physiological functions. These actions rely on tightly regulated temporal and concentration gradients of VEGF and VEGF receptor expression in the lung. Excessive or diminished VEGF have been linked to abnormal lung phenotypes and, in humans, linked to several diseases. The beneficial and detrimental actions of VEGF underscore that therapeutic targeting of VEGF in disease has to carefully consider the lung biology of VEGF.
PMCID: PMC2622735  PMID: 18468486
2.  Phagocytic clearance of apoptotic cells: role in lung disease 
Apoptosis and apoptotic clearance are matched processes that are centered in the maintenance of homeostasis. Similar to apoptosis, apoptotic cell clearance is a conserved mechanism that is highly efficient and redundant, highlighting its overall functional importance in homeostasis. Increasing evidence suggests that the mismatch between apoptosis and apoptotic cell clearance underlies pathologic conditions including inflammatory lung diseases, such as chronic obstructive pulmonary disease, cystic fibrosis, asthma, acute lung injury/acute respiratory distress syndrome and cancer immunity. Although direct causality has yet to be established, this paradigm opens novel approaches towards the understanding and treatment of lung diseases. Glucocorticoids, statins and macrolide antibiotics, which are already in use for treating lung conditions, have a positive effect on apoptotic clearance and are among novel agents that are potential candidates for treatment of these disorders.
PMCID: PMC3956128  PMID: 20477237
acute lung injury; apoptosis; apoptotic cell clearance; asthma; chronic obstructive Pulmonary disease; cystic fibrosis; efferocytosis; lung cancer; phagocytosis
3.  Cigarette Smoke Triggers Code Red 
The article by Yao and coworkers in this issue (Am. J. Respir. Cell Mol. Biol. 2008;39:7–18) reveals that the cyclin-dependent kinase inhibitor p21CIP1/WAF1/SDI1 (designated hereafter as p21), which has been linked to cell cycle growth arrest due to stress or danger cell responses, may modulate alveolar inflammation and alveolar destruction, and thus enlightens our present understanding of how the lung senses injury due to cigarette smoke and integrates these responses with those that activate inflammatory pathways potentially harmful to the lung (1). Furthermore, the interplay of p21 and cellular processes involving cell senescence and the imbalance of cell proliferation/apoptosis may provide us with a more logical explanation of how p21, acting as a sensor of cellular stress, might have such potent and wide roles in lung responses triggered by cigarette smoke. Molecular switches, ontologically designed for the protection of the host, are now hijacked by injurious stresses (such as cigarette smoke), leading to organ damage.
PMCID: PMC2720121  PMID: 18441278
4.  It takes two to tango: cigarette smoke partners with viruses to promote emphysema 
The Journal of Clinical Investigation  2008;118(8):2689-2693.
Viruses constitute a constant and renewed threat to humans. Not only do viruses cause disease directly due to their tissue tropism and pathogenicity, but they have also been linked to autoimmunity. In their study in this issue of the JCI, Kang et al. show that exposure to cigarette smoke induces alterations in the innate immune response to viral infection and that these changes hasten alveolar destruction characteristic of emphysema in mice (see the related beginning on page 2771). This study builds on evidence that patients with chronic obstructive pulmonary disease have clinical exacerbations associated with viral or bacterial infections, which lead to worsened lung function and increased mortality. This novel paradigm may aid related genetic, biomarker, and therapeutic developments and provides important insights into the pathogenesis of emphysematous lung destruction.
PMCID: PMC2483690  PMID: 18654673

Results 1-4 (4)