Cigarette smoke-associated inflammation impairs bone remodeling through NFκB activation.

Background: Cigarette smoking constitutes a major lifestyle risk factor for osteoporosis and hip fracture. It is reported to impair the outcome of many clinical procedures, such as wound infection treatment and fracture healing. Importantly, although several studies have already demonstrated the negative correlation between cigarette consume and impaired bone homeostasis, there is still a poor understanding of how does smoking affect bone health, due to the lack of an adequately designed animal model.

Lung carcinomas induced by NNK and LPS.

Cigarette smoking is the major culprit of chronic lung diseases and the most dominant risk factor for the development of both lung cancer and chronic obstructive pulmonary disease (COPD). In addition, chronic inflammation has been shown to increase the risk of lung cancer and COPD in clinical and epidemiological studies. For pulmonary disease-related research, mice are the most commonly used model system.

K-ras mutations in lung tumors from NNK-treated mice with lipopolysaccharide-elicited lung inflammation.

Background: Chronic lung inflammation has been associated with an increased risk of lung cancer. However, it is unclear whether such an event affects the incidence of mutations in the K-ras oncogene frequently found in lung tumors and suggested to be involved in lung tumorigenesis. This study investigated potential impacts of inflammation on the incidence of lung tumors and K-ras mutations using a mouse model.

Caveolin-1 expression is required for the development of pulmonary emphysema through activation of the ATM-p53-p21 pathway.

Free radicals play a role in aging and age-related human diseases, including pulmonary emphysema. Cigarette smoke represents a source of oxidants and is considered an environmental hazard that causes pulmonary emphysema. Here, we show that caveolin-1 activates ataxia telangiectasia-mutated (ATM) after oxidative stress by sequestering the ATM inhibitor, the catalytic subunit of protein phosphatase 2A, into caveolar membranes.