Cellular and mitochondrial calcium communication in obstructive lung disorders

Abstract

Calcium (Ca2+) signalling is well known to dictate cellular functioning and fate. In recent years, the accumulation of Ca2+ in the mitochondria has emerged as an important factor in Chronic Respiratory Diseases (CRD) such as Asthma and Chronic Obstructive Pulmonary Disease (COPD). Various reports underline an aberrant increase in the intracellular Ca2+, leading to mitochondrial ROS generation, and further activation of the apoptotic pathway in these diseases. Mitochondria contribute to Ca2+ buffering which in turn regulates mitochondrial metabolism and ATP production. Disruption of this Ca2+ balance leads to impaired cellular processes like apoptosis or necrosis and thus contributes to the pathophysiology of airway diseases. This review highlights the key role of cytoplasmic and mitochondrial Ca2+ signalling in regulating CRD, such as asthma and COPD. A better understanding of the dysregulation of mitochondrial Ca2+ homeostasis in these diseases could provide cues for the development of advanced therapeutic interventions in these diseases.