Gliomas are the most fatal malignant cerebral tumors. Temozolomide (TMZ), as the primary chemotherapy drug, has been widely used in clinics. However, resistance of TMZ still remains to poor defined. LncRNAs have been reported to play crucial roles in progression of various cancers and resistance of multiple drugs. However, the biological function and underlying mechanisms of most lncRNAs in glioma still remains unclear. Based on the TCGA database, a total of 94 differentially expressed lncRNAs, including 16 up-regulated genes and 78 downregulated genes were identified between gliomas and normal brain tissues. Subsequently, lncRNA DLEU1, HOTAIR, and LOC00132111 were tested to be significantly related to overall survival (OS) between high- and low-expression groups. Additionally, we verified that lncRNA DLEU1 was high expressed in 108 gliomas, compared with 19 normal brain tissues. And high expression of lncRNA DLEU1 predicted a poor prognosis (HR = 1.703, 95%CI 1.133-2.917, p-value = 0.0159). Moreover, functional assays revealed that knockdown of lncRNA DLEU1 could suppress the proliferation by inducing cell cycle arrest at G1 phase and reducing the S phase by down-regulating the CyclinD1 and p-AKT, as the well as migration and invasion by inhibiting the epithelial-mesenchymal transition (EMT) markers, such as ZEB1, N-cadherin, β-catenin and snail in glioma cells. Furthermore, silencing lncRNA DLEU1 suppressed TMZ-activated autophagy via regulating the expression of P62 and LC3, and promoted sensitivity of glioma cells to TMZ by triggering apoptosis. Conclusively, our study indicated that lncRNA DLEU1 might perform as a prognostic potential target and underlying therapeutic target for sensitivity of glioma to TMZ.Disruption of mitochondrial biosynthesis or dynamics, or loss of control over mitochondrial regulation leads to a significant alteration in fuel preference and metabolic shifts that potentially affect the health of kidney cells. Mitochondria regulate metabolic networks which affect multiple cellular processes. Indeed, mitochondria have established themselves as therapeutic targets in several diseases. The importance of mitochondria in regulating the pathogenesis of several diseases has been recognized, however, there is limited understanding of mitochondrial biology in the kidney. This review provides an overview of mitochondrial dysfunction in kidney diseases. We describe the importance of mitochondria and mitochondrial sirtuins in the regulation of renal metabolic shifts in diverse cells types, and review this loss of control leads to increased cell-to-cell transdifferentiation processes and myofibroblast-metabolic shifts, which affect the pathophysiology of several kidney diseases. In addition, we examine mitochondrial-targeted therapeutic agents that offer potential leads in combating kidney diseases.Scutellarin (SCU) is an active ingredient extracted from Erigeron breviscapus (Vaniot) Hand.-Mazz. Its main physiological functions are anti-inflammatory and antioxidant. In this study, we established a STZ-induced model of type 2 diabetes (T2DM) and a homocysteine (Hcy)-induced apoptosis model of LO2 to investigate whether SCU can alleviate liver damage by regulating Hcy in type 2 diabetes. Biochemical analysis indicated that SCU could improve the lipid metabolism disorder and liver function in diabetic rats by downregulating the levels of triglycerides (TG), cholesterol (CHO), low-density lipoprotein (LDL), alanine transaminase (ALT) and aspartate transaminase (AST), and by upregulating the level of high-density lipoprotein (HDL). Interestingly, SCU also could down-regulate the levels of Hcy and insulin and enhance the ability of type 2 diabetic rats to regulate blood glucose. Mechanistically, our results indicated that SCU may control the level of Hcy through regulating the levels of β-Cystathionase (CBS), γ-Cystathionase (CSE) and 5,10-methylenetetrahydrofolate (MTHFR) in liver tissue, and up-regulate folic acid, VitB6 and VitB12 levels in serum. Furthermore, SCU inhibits apoptosis in the liver of T2DM rats and in cultured LO2 cells treated with Hcy. Together, our findings suggest that SCU may alleviate the liver injury thorough downregulating the level of Hcy in T2DM rats.Acute myeloid leukemia (AML) is an aggressive haematological malignancy characterized by highly proliferative accumulation of immature and dysfunctional myeloid cells. Quercetin (Qu), one kind of flavonoid, exhibits anti-cancer property in multiple types of solid tumor, but its effect on acute myeloid leukemia is less studied, and the underlying mechanisms still largely unknown. This study aimed to explore the specific target and potential mechanism of quercetin-induced cell death in AML. First, we found that quercetin induces cell death in the form of apoptosis, which was caspase dependent. Second, we found that quercetin-induced apoptosis depends on the decrease of mitochondria membrane potential (MMP) and Bcl-2 proteins. With quantitative chemical proteomics, we observed the downregulation of VEGFR2 and PI3K/Akt signaling in quercetin-treated cells. Consistently, cell studies also identified that VEGFR2 and PI3K/Akt signaling pathways are involved in the action of quercetin on mitochondria and Bcl-2 proteins. The decrease of MMP and cell death could be rescued when PI3K/Akt signaling is activated, suggesting that VEGFR2 and PI3K/Akt exert as upstream regulators for quercetin effect on apoptosis induction in AML cells. In conclusion, our findings from this study provide convincing evidence that quercetin induces cell death via downregulation of VEGF/Akt signaling pathways and mitochondria-mediated apoptosis in AML cells.Mitochondria are essential cellular organelles that act as metabolic centers and signaling platforms and have been identified as an important subcellular target in a broad range of neuropathologies. Studies on the role of mitochondria in neurological disorders have primarily focused on neurons. However, dysfunctional mitochondria in glial cells, particularly astrocytes, have recently gained research attention due to their close involvement in neuroinflammation and metabolic and neurodegenerative disorders. selleck inhibitor Furthermore, alterations in mitochondrial energy metabolism in astrocytes have been reported to modulate cellular morphology and activity and induce the release of diverse proinflammatory mediators. Moreover, emerging evidence suggests that dysregulation of mitochondrial dynamics characterized by aberrant fission and fusion events in glial cells is closely associated with the inflammatory activation of glia. In this mini-review, we cover the recent advances in the molecular aspects of astrocytic mitochondrial dynamics and their metabolic changes under the pathological conditions of the central nervous system (CNS).