Mitochondrial membrane potential and the generation of reactive oxygen species (ROS) were used as functional indexes of mitochondria dysfunction. Bcl‑2 and caspase‑3 expression levels were analyzed by western blotting. The present results suggested that moderate hypothermia significantly increased SUMO1 and Bcl‑2 expression levels, as well as the mitochondrial membrane potential, but significantly decreased the expression levels of caspase‑3 and mitochondrial ROS. Thus, moderate hypothermia may enhance SUMOylation and attenuate myocardial H/R injury. Moreover, a combination of SUMOylation and moderate hypothermia may be a potential cardiovascular intervention.Autophagy is activated under radiation stress, which serves an important role in maintaining bone homeostasis. However, the underlying mechanisms of irradiation‑induced autophagy in bone homeostasis is not well understood.  https://www.selleckchem.com/products/ziftomenib.html  The present study aimed to determine the effects of radiation‑activated autophagy on pre‑osteoblastic MC3T3‑E1 cells. X‑ray irradiation activated autophagy in a dose‑dependent manner, with an increased fluorescence intensity of monodansylcadaverine staining, increased ratio of microtubule‑associated protein 1 light chain 3β (LC3)‑II/LC3‑I, decreased p62 expression, and increased ATG5 and beclin‑1 expression levels in MC3T3‑E1 cells 72 h after irradiation compared with those in non‑irradiated MC3T3‑E1 cells. Irradiation reduced colony formation and mineralization in a dose‑dependent manner in MC3T3‑E1 cells at 2 and 3 weeks after irradiation, respectively. Decreased levels of alkaline phosphatase activity and runt‑related transcription factor 2 expression were observed at 72 h post‑irradiation. In addition, irradiation‑induced apoptosis was accompanied by a decreased ratio of Bcl‑2/BAX protein and increased the activity of caspase‑3. By contrast, doxycycline (DOX)‑inhibited autophagy attenuated the decreased colony formation and mineralization, and aggravated the increased cell apoptosis in irradiated MC3T3‑E1 cells. Furthermore, the ratio of phosphorylated P38/P38 was observed to be higher following DOX treatment within 1 week of irradiation, which was reversed 2 weeks post‑irradiation. In conclusion, DOX‑inhibited autophagy aggravated X‑ray irradiation‑induced apoptosis at an early stage, but maintained cell proliferation and mineralization at a late stage in irradiated MC3T3‑E1 cells.Lung adenocarcinoma (LUAD), a major subtype of lung cancer, is the leading cause of cancer‑related mortality worldwide. Previous studies have determined the role of the protein arginine methyltransferases (PRMTs) in the physiology and pathology of LUAD. However, to the best of our knowledge, no empirical studies have been performed determining the association between protein arginine methyltransferase 6 (PRMT6) and LUAD. The present study aimed to determine the expression levels of PRMT6 in LUAD and its association with the clinicopathological characteristics. The effect of PRMT6 knockdown on cell growth was analyzed and chromatin immunoprecipitation (ChIP) assay was used to investigate the regulatory mechanisms of PRMT6 on downstream gene expression. In addition, a xenograft model was used to determine whether the PRMT6‑regulated expression levels of p18 in vitro could be validated in vivo. PRMT6 overexpression in LUAD is associated with high clinical stage, lymph node metastasis and poor clinical outcomes. Furthermore, the silencing of PRMT6 significantly reduced the enrichment of Histone H3 asymmetric demethylation at arginine 2 in the promoter region of the p18 gene, thereby activating the expression of the gene. This, in turn, induced G1/S phase cell cycle arrest, resulting in the inhibition of cell proliferation. The xenograft model also suggested that PRMT6 suppressed LUAD development by activating p18 expression in vivo. In conclusion, the findings of the present study suggested that PRMT6 may serve as an oncogene in the progression of LUAD through epigenetically suppressing p18 expression. Thus, PRMT6 may represent a novel potential therapeutic target for LUAD.The occurrence and development of hyperglycemia‑induced inflammation is associated with increased expression of receptor for advanced glycation end products (RAGE) and inflammatory factors, including IL‑1β, TNF‑α and IL‑6. Previous studies have reported that the nucleotide‑binding oligomerization domain‑like receptor protein 3 (NLRP3) inflammasome interacts with thioredoxin‑interacting protein (TXNIP) and serves a crucial role in inflammation. FPS‑ZM1 has been identified as target inhibitor of RAGE and has been shown to exert an anti‑inflammatory effect in vitro. However, the underlying mechanism by which FPS‑ZM1 impacts high glucose (HG)‑induced inflammation in bone marrow mesenchymal stem cells (BMSCs) remains unclear. The present study explored the regulatory effect of FPS‑ZM1 on HG‑induced inflammation in BMSCs. Furthermore, the role of the TXNIP/NLRP3 inflammasome signaling pathway in the regulatory effects of FPS‑ZM1 on HG‑induced inflammation was studied. Cell viability was determined using Cell Countimmasome signaling pathway mediated the molecular mechanism underlying this effect.Hepatic fibrosis (HF) is a common complication of numerous chronic liver diseases, but predominantly results from persistent liver inflammation or injury. If left untreated, HF can progress and develop into liver cirrhosis and even hepatocellular carcinoma. However, the underlying molecular mechanisms of HF remain unknown. The present study aimed to investigate the role of 11β‑hydroxysteroid dehydrogenase‑1 (11β‑HSD1) during the development of hepatic fibrosis. An experimental rat model of liver fibrosis was induced using porcine serum. 11β‑HSD1 gene expression levels and enzyme activity during hepatic fibrogenesis were assessed. 11β‑HSD1 gene knockdown using small interfering RNA and overexpression were performed in LX2‑human hepatic stellate cells (HSCs). HSCs were stimulated with transforming growth factor‑β1 (TGF‑β1). Cell cycle distribution, proliferation, collagen secretion and 11β‑HSD1 gene activity in HSCs were compared before and after stimulation. As hepatic fibrosis progressed, 11β‑HSD1 gene expression and activity increased, indicating a positive correlation with typical markers of liver fibrosis.