Narala Venkata Ramireddy, Narala Sahithi Reddy, Aiya Subramani Parasuraman, Panati Kalpana, Kolliputi Narasaiah
Department of Zoology, Yogi Vemana University, Kadapa, India.
Kurnool Medical College, Kurnool, India.
Front Pharmacol. 2024 Aug 20;15:1433961. doi: 10.3389/fphar.2024.1433961. eCollection 2024.
Mitochondria play a significant and varied role in inflammatory lung disorders. Mitochondria, known as the powerhouse of the cell because of their role in producing energy, are now recognized as crucial regulators of inflammation and immunological responses. Asthma, chronic obstructive pulmonary disease, and acute respiratory distress syndrome are characterized by complex interactions between immune cells, inflammatory substances, and tissue damage. Dysfunctional mitochondria can increase the generation of reactive oxygen species (ROS), triggering inflammatory pathways. Moreover, mitochondrial failure impacts cellular signaling, which in turn affects the expression of molecules that promote inflammation. In addition, mitochondria have a crucial role in controlling the behavior of immune cells, such as their activation and differentiation, which is essential in the development of inflammatory lung diseases. Their dynamic behavior, encompassing fusion, fission, and mitophagy, also impacts cellular responses to inflammation and oxidative stress. Gaining a comprehensive understanding of the intricate correlation between mitochondria and lung inflammation is essential in order to develop accurate treatment strategies. Targeting ROS generation, dynamics, and mitochondrial function may offer novel approaches to treating inflammatory lung diseases while minimizing tissue damage. Additional investigation into the precise contributions of mitochondria to lung inflammation will provide significant knowledge regarding disease mechanisms and potential therapeutic approaches. This review will focus on how mitochondria in the lung regulate these processes and their involvement in acute and chronic lung diseases.
线粒体在炎症性肺部疾病中发挥着重要且多样的作用。线粒体因其在产生能量方面的作用而被称为细胞的动力源,现在被认为是炎症和免疫反应的关键调节因子。哮喘、慢性阻塞性肺疾病和急性呼吸窘迫综合征的特征是免疫细胞、炎症物质和组织损伤之间的复杂相互作用。功能失调的线粒体可增加活性氧(ROS)的产生,触发炎症途径。此外,线粒体功能障碍会影响细胞信号传导,进而影响促进炎症的分子的表达。此外,线粒体在控制免疫细胞的行为方面起着关键作用,例如它们的激活和分化,这在炎症性肺部疾病的发展中至关重要。它们的动态行为,包括融合、裂变和线粒体自噬,也会影响细胞对炎症和氧化应激的反应。全面了解线粒体与肺部炎症之间的复杂关联对于制定准确的治疗策略至关重要。针对ROS的产生、动态变化和线粒体功能可能提供治疗炎症性肺部疾病的新方法,同时将组织损伤降至最低。对线粒体对肺部炎症的确切贡献的进一步研究将提供有关疾病机制和潜在治疗方法的重要知识。本综述将重点关注肺部线粒体如何调节这些过程以及它们在急性和慢性肺部疾病中的作用。