Cellular and mitochondrial calcium communication in obstructive lung disorders

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.