https://www.selleckchem.com/products/bardoxolone.html Besides, shRNA-mediated Kiaa0101 knockdown inhibited migration and invasion of glioma cells by reducing snail1 expression both and , whereas its upregulation enhanced malignant behaviors of these cells. Furthermore, Kiaa0101 regulated snail1 expression by activating the p38MAPK signaling pathway. Our findings strongly indicate that Kiaa0101 is a prognostic biomarker for malignant tumors, and its inhibition may be an effective strategy for treating glioma. Our findings strongly indicate that Kiaa0101 is a prognostic biomarker for malignant tumors, and its inhibition may be an effective strategy for treating glioma. Mitochondrial dysfunction plays an important role in the development of septic cardiomyopathy. This study aimed to reveal the protective role of uncoupling protein 2 (UCP2) in mitochondria through AMP-activated protein kinase (AMPK) on autophagy during septic cardiomyopathy. UCP2 knockout mice via a cecal ligation and puncture (CLP) model and the H9C2 cardiomyocyte cell line in response to lipopolysaccharide (LPS) were used to study the effect. The myocardial morphological alterations, indicators of mitochondrial injury and levels of autophagy-associated proteins (pAMPK, pmTOR, pULK1, pTSC2, Beclin-1, and LC3-I/II) were assessed. In addition, the mechanism of the interaction between UCP2 and AMPK was further studied through gain- and loss-of-function studies. Compared with the wild-type mice, the UCP2 knockout mice exhibited more severe cardiomyocyte injury after CLP, and the AMPK agonist AICAR protected against such injury. Consistent with this result, silencing UCP2 augmented the LPS-induced pathological damage and mitochondrial injury in the H9C2 cells, limited the upregulation of autophagy proteins and reduced AMPK phosphorylation. AICAR protected the cells from morphological changes and mitochondrial membrane potential loss and promoted autophagy. The silencing and overexpression of UCP2 led to cor