Uridine is one of the essential nutrients in organisms. To maintain normal cell growth and intracellular metabolism, the uridine must be maintained at certain concentration. Recent studies have shown that uridine can reduce inflammatory response in organisms, participate in glycolysis, and regulate intracellular protein modification, such as glycosylation and acetylation. Furthermore, it can protect cells from hypoxic injury by reducing intracellular oxidative stress, promoting high-energy compounds synthesis. Previous studies have shown that the protective effects of uridine are closely related to its effect on mitochondria. This review summarizes the effect of uridine on mitochondrial function.
Uridine/metabolism* ; Mitochondria/metabolism*

Remodeling of the mitochondrial network is an important process in the maintenance of cellular homeostasis and is closely related to mitochondrial function. Interactions between the biogenesis of new mitochondria and the clearance of damaged mitochondria (mitophagy) is an important manifestation of mitochondrial network remodeling. Mitochondrial fission and fusion act as a bridge between biogenesis and mitophagy. In recent years, the importance of these processes has been described in a variety of tissues and cell types and under a variety of conditions. For example, robust remodeling of the mitochondrial network has been reported during the polarization and effector function of macrophages. Previous studies have also revealed the important role of mitochondrial morphological structure and metabolic changes in regulating the function of macrophages. Therefore, the processes that regulate remodeling of the mitochondrial network also play a crucial role in the immune response of macrophages. In this paper, we focus on the molecular mechanisms of mitochondrial regeneration, fission, fusion, and mitophagy in the process of mitochondrial network remodeling, and integrate these mechanisms to investigate their biological roles in macrophage polarization, inflammasome activation, and efferocytosis.
Mitochondria ; Mitophagy ; Homeostasis/physiology* ; Phagocytosis ; Macrophages/metabolism*

Apoptosis ; Proteins/metabolism* ; Mitochondria/metabolism* ; CD4-Positive T-Lymphocytes

Cadmium/metabolism* ; Kidney ; Cells, Cultured ; Mitochondria ; Metallothionein/metabolism* ; Liver

The effects of 7-ethyl-8-methylf1avin (7-Et) and 7-methyl-8-ethyl-flavin (8-Et) on rat hepatic monoamine oxidase (MAO), brain MAO activity and 5-hydroxytryptamine (5-HT or serotonin) in rat brain were investigated. In the study of hepatic MAO activity, kynur-amine a nonphysiological substrate for both A and B type MAO, was used for a spectro-photometric method, and [14C]-labeled amines were also used for a radiometric procedure for camparison with MAO activity determined by the spectrophotometric method. The rate of change in MAO activity of hepatic mitochondria from rats receiving Rb-def and 7-Et and 8-Et flavin showed the activity was severely reduced during 8 weeks. Rapid reduction of enzyme activity (50% in def-group, 35% in 7-Et group and 8% 8-Et flavin group) was observed at the end of 2 weeks. The enzyme activity lasted with slow decre-ment of enzyme level from 4 weeks to the end of 8 weeks as low as 16% in def, 18% in 7-Et and 3% in 8-Et flavin group. The trend of decrement of MAO activity when kynura-mine was used as a substrate appears to be similar with the small variation of MAO activity when [14C]-labelled tyramine, dopamine, serotonin and tryptamine respectively were used as substrate. The rate of decay of brain mitochondrial MAO activity in rats receiving each respective f1avin was not rapid and severely depressed as the MAO activity we have found in liver mitochondrial MAO of rats during the 8 week experimental time, but a similar tendency of decay of MAO in each group was observed. The potent inhibitory effect of 8-Et on brain MAO was confirmed by the study of the simultaneous measure-ment of MAO activity in each experimental group. when the reduction Of brain MAO activity in rats receiving 8-Et after 6 weeks was approximately 80% of normal and in the same rats the concentration of brain 5-HT showed a 60% increment of that of the normal mts. During the experimental period there is no absolute parallelism between the MAO inhibition and 5-HT increase. However when the reduction of MAO activity reached 80% of normal value, the concentration of 5-HT increased dramatically as much as 60% of normal value. The results so far suggest clearly that 8-Et produces a much more potent inhibitory effect on the hepatic MAO a s well as brain MAO in rats. Therefore our present and previous results suggest that 7-Et and 8-Et flavin should bind itself to hepatic, brain MAO apoenzyme in the condition of total absence of riboflavin in these animals, and the holenzyme is catalytically inactive.
Animal ; Brain/enzymology* ; Brain/metabolism ; Comparative Study ; Male ; Mitochondria/enzymology* ; Mitochondria, Liver/enzymology* ; Monoamine Oxidase/metabolism* ; Rats ; Serotonin/metabolism*

Liver plays a central role in the biogenesis of major metabolites including glucose, fatty acids, and cholesterol. Increased incidence of obesity in the modern society promotes insulin resistance in the peripheral tissues in humans, and could cause severe metabolic disorders by inducing accumulation of lipid in the liver, resulting in the progression of non-alcoholic fatty liver disease (NAFLD). NAFLD, which is characterized by increased fat depots in the liver, could precede more severe diseases such as non-alcoholic steatohepatitis (NASH), cirrhosis, and in some cases hepatocellular carcinoma. Accumulation of lipid in the liver can be traced by increased uptake of free fatty acids into the liver, impaired fatty acid beta oxidation, or the increased incidence of de novo lipogenesis. In this review, I would like to focus on the roles of individual pathways that contribute to the hepatic steatosis as a precursor for the NAFLD.
Acetyl Coenzyme A/metabolism ; Fatty Acids/metabolism ; Fatty Liver/*metabolism/pathology ; Humans ; Lipogenesis ; Mitochondria/metabolism ; Triglycerides/metabolism

OBJECTIVE: To 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.
Humans ; Reactive Oxygen Species/metabolism* ; Chondrocytes/metabolism* ; Osteoarthritis/metabolism* ; Homeostasis ; Mitochondria/metabolism* ; Cartilage, Articular/metabolism*

Metabolic syndrome and diabetes are associated with increased risk of cardiac dysfunction independently of underlying coronary artery disease. The underlying pathogenesis is partially understood but accumulating evidence suggests that alterations of cardiac energy metabolism might contribute to the development of contractile dysfunction. Recent findings suggest that myocardial mitochondrial dysfunction may play an important role in the pathogenesis of cardiac contractile dysfunction in type 2 diabetes. This review is focused on evaluating mechanisms for the mitochondrial abnormalities that may be involved in the development and progression of cardiac dysfunction in diabetes.
Coronary Artery Disease ; Diabetic Cardiomyopathies ; Energy Metabolism ; Mitochondria

Photobiomodulation utilizes monochromatic (or quasimonochromatic) light in the electromagnetic region of 600~1000 nm for the treatment of soft tissues in a nondestructive and nonthermal mode. It is conceivable that photobiomodulation is based upon the ability of the light to alter cell metabolism as it is absorbed by general hemoproteins and cytochrome c oxidase (COX) in particular. Recently it has been suggested radiation of visible and infrared (IR) activates retrograde signaling pathway from mitochondria to nucleus. In this review, the role of COX in the photobiomodulation will be discussed. Further a possible role of water as a photoreceptor will be suggested.
Electron Transport Complex IV ; Magnets ; Metabolism ; Mitochondria ; Phototherapy* ; Water

Electron Transport ; Electron Transport Complex III ; deficiency ; Humans ; Mitochondria ; metabolism