Anup Srivastava, Ph.D.

Cigarette smoking is the primary risk factor for COPD, which is characterized by excessive inflammation and airflow obstruction of the lung. The mechanisms underlying these inflammatory responses are poorly understood. The factors affecting the health of mitochondria the microscopic ""power plants"" inside cells that produce the energy that runs the body have important roles in inflammation and cigarette smoke?induced COPD. We will study dysfunction of the mitochondria and how that leads to COPD. We will focus on a protein involved in mitochondrial function called MKK3. We believe that targeting MKK3 may have substantial therapeutic effects in cigarette smoke-induced COPD. The results could lead to the discovery of novel treatments for COPD.

Update: Our research is consolidating our hypothesis that MKK3 is a central player in modulating mitochondrial function and inflammation in cigarette smoke-induced COPD and that a potential target for treatment. We have exposed mice deficient in MKK3 and mice with the protein to cigarette smoke, and are analyzing the samples. We are continuing to analyze the mechanism of cigarette smoke-induced inflammation and the role of MKK3, and to identify potential therapeutic approaches.