The role of SESTRINs in Chronic Obstructive Pulmonary Disease

Chronic Obstructive Pulmonary Disease (COPD) is the major cause of morbidity and mortality worldwide with no efficient cure.

COPD is tightly linked with tobacco smoke exposure that induces stress response in lung parenchymal cells and this response contributes to the development of the disease. We have previously characterised a stress-regulated SESTRIN gene family and determined that SESTRINs can be involved in stress response associated with tobacco smoke exposure. SESTRINS are major suppressors of mammalian target of rapamycin complex 1 kinase responsible for control of metabolism, autophagy and cell viability.

We propose that SESTRINS might be involved in the development of COPD through control of metabolism and cell death. In this work we will determine the impact of SESTRINs on regulation of physiological and pathophysiological processes in lung epithelial cells in response to tobacco smoke exposure and define whether inactivation of SESTRIN proteins can be a strategy for COPD treatment.