With the increasing appreciation of mitochondria in modulating cellular homeostasis, various disease biology researchers have started exploring the detailed role of mitochondria in multiple diseases beyond neuronal and muscular diseases. In this context, emerging shreds of evidence in lung biology indicated the meticulous role of lung epithelia in provoking a plethora of lung diseases in contrast to earlier beliefs. As lung epithelia are ceaselessly exposed to the environment, they need to have multiple protective mechanisms to maintain the integrity of lung structure and function. As ciliated airway epithelium and type 2 alveolar epithelia require intense energy for executing their key functions like ciliary beating and surfactant production, it is no surprise that defects in mitochondrial function in these cells could perturb lung homeostasis and engage in the pathophysiology of lung diseases. On one hand, intracellular calcium plays a central role in executing key functions of lung epithelia, and on the other hand maintenance of intracellular calcium needs the buffering role of mitochondria. Thus, the regulation of mitochondrial calcium in lung epithelia seems to be critical in lung homeostasis and could be decisive in the pathogenesis of various lung diseases.

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线粒体钙在决定肺上皮完整性和肺病病理生理学中的潜在作用

随着线粒体在调节细胞内稳态方面的作用越来越受到重视，各种疾病生物学研究人员已经开始探索线粒体在神经元和肌肉疾病以外的多种疾病中的详细作用。在这种情况下，肺生物学中出现的大量证据表明，与早期的看法相反，肺上皮细胞在引发过多肺部疾病方面的细致作用。由于肺上皮不断暴露在环境中，它们需要具有多种保护机制来维持肺结构和功能的完整性。由于纤毛气道上皮细胞和 2 型肺泡上皮细胞需要大量能量来执行它们的关键功能，如纤毛跳动和表面活性剂的产生，毫不奇怪，这些细胞中线粒体功能的缺陷会扰乱肺稳态并参与肺部疾病的病理生理学。一方面，细胞内钙在执行肺上皮的关键功能中起着核心作用，另一方面，细胞内钙的维持需要线粒体的缓冲作用。因此，肺上皮细胞中线粒体钙的调节似乎对肺稳态至关重要，并且可能在各种肺部疾病的发病机制中起决定性作用。