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Pharmacy reseacher studies lung damage in former smokers

Even after they stop smoking, patients with chronic obstructive pulmonary disease continue to experience lung damage.

Enrique Cadenas, the Charles Krown Alumni Professor in Pharmaceutical Sciences and associate dean for research affairs at the School of Pharmacy, has received a grant of $394,380 over three years from the Tobacco-Related Disease Research Program to study emphysema associated with chronic obstructive pulmonary disease.

The study examines the observation that apoptosis, or cell death, continues to occur in patients with the disease even after they have stopped smoking. Cadenas will explore the idea that once mitochondria are damaged by smoking, a vicious cycle is unleashed that spreads and intensifies the already damaging effects of cigarette smoke.

“This impairment of mitochondrial function ultimately causes cell death, which often leads to emphysema,” Cadenas said. “During the course of the project, we will consider compounds that can offset this destruction by improving mitochondrial function and thus halt or minimize the damaging effects of past smoking.”

Chronic obstructive pulmonary disease damages and obstructs the lung airways, making it hard to breathe. Cigarette smoking is commonly associated with the disease, causing more than 90 percent of the cases. It is estimated that more than 24 million Americans have the disease, many of them undiagnosed.

The Tobacco-Related Disease Research Program was created in California in 1989. Funded by cigarette surtax revenues, the program supports research projects on tobacco-related diseases.

Cadenas is known for his work on cellular dysfunction in the aging process and age-related, degenerative diseases. His work considers events that produce free radical injury and the development of therapeutic models that prevent free radical damage and the effects of aging.

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