Search

As important organelles of energetic and metabolism, changes in the dynamic state of mitochondria affect the homeostasis of cellular metabolism. Mitochondrial dynamics include mitochondrial fusion and mitochondrial fission. The former is coordinated by mitofusin-1 (Mfn1), mitofusin-2 (Mfn2), and optic atrophy 1 (Opa1), and the latter is mediated by dynamin related protein 1 (Drp1), mitochondrial fission 1 (Fis1) and mitochondrial fission factor (MFF). Mitochondrial fusion and fission are generally in dynamic balance and this balance is important to preserve the proper mitochondrial morphology, function and distribution. Diabetic conditions lead to disturbances in mitochondrial dynamics, which in return causes a series of abnormalities in metabolism, including decreased bioenergy production, excessive production of reactive oxygen species (ROS), defective mitophagy and apoptosis, which are ultimately closely linked to multiple chronic complications of diabetes. Multiple researches have shown that the incidence of diabetic complications is connected with increased mitochondrial fission, for example, there is an excessive mitochondrial fission and impaired mitochondrial fusion in diabetic cardiomyocytes, and that the development of cardiac dysfunction induced by diabetes can be attenuated by inhibiting mitochondrial fission. Therefore, targeting the restoration of mitochondrial dynamics would be a promising therapeutic target within type II diabetes (T2D) and its complications. The molecular approaches to mitochondrial dynamics, their impairment in the context of T2D and its complications, and pharmacological approaches targeting mitochondrial dynamics are discussed in this review and promise benefits for the therapy of T2D and its comorbidities. [ABSTRACT FROM AUTHOR]

Worldwide, the rapid increase in the incidence of diabetes and its complications poses a serious threat to human health. Ferroptosis, which is a new nonapoptotic form of cell death, has been proven to be closely related to the occurrence and development of diabetes and its complications. In recent years, lncRNAs have been confirmed to be involved in the occurrence and development of diabetes and play an important role in regulating ferroptosis. An increasing number of studies have shown that lncRNAs can affect the occurrence and development of diabetes and its complications by regulating ferroptosis. Therefore, lncRNAs have great potential as therapeutic targets for regulating ferroptosis-mediated diabetes and its complications. This paper reviewed the potential impact and regulatory mechanism of ferroptosis on diabetes and its complications, focusing on the effects of lncRNAs on the occurrence and development of ferroptosis-mediated diabetes and its complications and the regulation of ferroptosis-inducing reactive oxygen species, the key ferroptosis regulator Nrf2 and the NF-κB signaling pathway to provide new therapeutic strategies for the development of lncRNA-regulated ferroptosis-targeted drugs to treat diabetes. [ABSTRACT FROM AUTHOR]

The mechanism of lignin degradation via white rot fungi was studied. Phanerochaete chrysosporium and Pleurotus ostreatus were used for all the experiments, i.e., measuring the concentration and structure of alkali lignins and studying the effect of the substrate concentration and enzyme activity on the removal. Gas chromatography-mass spectrometry was performed on the reaction liquid of the lignin degradation enzyme system. Alkali lignin had a characteristic absorption spectrum with a peak at approximately 280 nm. Precipitation in the laccase (Lac) degradation system occurred earlier, as well as being more obvious than that in the manganese peroxidase (Mnp) degradation system. The maximum removal was 29.4% in the Mnp degradation system at a concentration of 40 mg/L. The removal increased in a concentration-dependent manner in the Lac degradation system. The increase in Mnp and Lac enzyme activity led to an increased alkali lignin removal. The removal of the control group was significantly lower than the experimental degradation systems. The degradation mainly produced organic acids, esters, and aromatic substances. In conclusion, white rot fungi could effectively remove alkali lignin, in which precipitation played a major role, followed by enzymolysis; the enzymolysis was associated with the alkali lignin concentration and enzyme activity. [ABSTRACT FROM AUTHOR]