ObjectiveTo summarize the role of chondrocyte mitochondrial homeostasis imbalance in the pathogenesis of osteoarthritis (OA) and analyze its application prospects. Methods The recent literature at home and abroad was reviewed to summarize the mechanism of mitochondrial homeostasis imbalance, the relationship between mitochondrial homeostasis imbalance and the pathogenesis of OA, and the application prospect in the treatment of OA. Results Recent studies have shown that mitochondrial homeostasis imbalance, which is caused by abnormal mitochondrial biogenesis, the imbalance of mitochondrial redox, the imbalance of mitochondrial dynamics, and damaged mitochondrial autophagy of chondrocytes, plays an important role in the pathogenesis of OA. Abnormal mitochondrial biogenesis can accelerate the catabolic reaction of OA chondrocytes and aggravate cartilage damage. The imbalance of mitochondrial redox can lead to the accumulation of reactive oxygen species (ROS), inhibit the synthesis of extracellular matrix, induce ferroptosis and eventually leads to cartilage degradation. The imbalance of mitochondrial dynamics can lead to mitochondrial DNA mutation, decreased adenosine triphosphate production, ROS accumulation, and accelerated apoptosis of chondrocytes. When mitochondrial autophagy is damaged, dysfunctional mitochondria cannot be cleared in time, leading to ROS accumulation, which leads to chondrocyte apoptosis. It has been found that substances such as puerarin, safflower yellow, and astaxanthin can inhibit the development of OA by regulating mitochondrial homeostasis, which proves the potential to be used in the treatment of OA. Conclusion The mitochondrial homeostasis imbalance in chondrocytes is one of the most important pathogeneses of OA, and further exploration of the mechanisms of mitochondrial homeostasis imbalance is of great significance for the prevention and treatment of OA.
Objective To investigate the role of mitochondrial autophagy mediated by PINK1 (homologous phosphatase tensin induced kinase 1) /Parkin (Parkinson’s protein) signaling pathway in severe pneumonia of rats. Methods Twenty rats were randomly divided into control group and model group (severe pneumonia model), with 10 rats in each group, to explore the effects of severe pneumonia on lung function and pathology in rats. Then, 30 rats were randomly divided into control group, model group and mdivi-1 (mitochondrial autophagy inhibitor) group, with 10 rats in each group, to further explore the effects of severe pneumonia on mitochondrial autophagy indicators of rats. ResultsCompared with the control group, the resting ventilation volume [(3.44±0.22) vs. (1.58±0.18) mL/min] and airway resistance ratio (77.48±3.84 vs. 47.76±5.54) in the model group were decreased (P<0.05). In the model group, the lung tissue was injured and a large number of inflammatory cells were infiltrated. The protein and mRNA expression levels of Parkin, PINK1 and microtubule-associated protein1 light chain 3 in lung tissues of model group were increased (P<0.05). Compared with model group, the ratio of resting ventilator-to-airway resistance in mdivi-1 group increased (P<0.05). The injury and inflammatory infiltration of lung tissue were improved in mdivi-1 group. The expression levels of Parkin, PINK1 and microtubule-associated protein1 light chain 3 protein and mRNA in lung tissues of mdivi-1 group were decreased (P<0.05). Conclusion Mdivi-1 can improve the abnormal lung function structure in rats with severe pneumonia, and the mechanism may be related to mitochondrial autophagy mediated by PINK1/Parkin signaling pathway.