RESUMO
With the increasingly rapid pace of updates and iterations in electronic devices, electronic equipment/systems are becoming progressively intricate, aiming to achieve swift responsiveness through higher packaging density, which leads to electromagnetic interference and brings along with it heat accumulation, the creation of new composite phase change materials with efficient thermal management capabilities integrated with excellent electromagnetic interference shielding capabilities is imminent. In this study, nickel foam/lignin/rGO dual network scaffolds (LGN) with high electrical conductivity were prepared by vacuum-assisted adsorption, freeze-drying, and thermal annealing, and then PEG was encapsulated in LGN by vacuum impregnation to obtain shape-stabilized PEG/NiF/LN-rGO (PLGN) composite phase change material. The results demonstrate that the prepared PLGNs exhibit robust stability, exceptional thermal management capabilities, and commendable electromagnetic interference (EMI) shielding effectiveness (SE). Among these composites, PLGN-3 stands out with a notably high energy storage density, featuring a melting enthalpy of 140.95â¯J/g and a relative enthalpy efficiency of 98.72â¯%. Benefiting from its outstanding electrical conductivity (1597.5â¯S/cm for PLGN-3) and superior light absorption, the PLGN composite phase change material also demonstrates highly effective photothermal and electrothermal conversion capabilities. In addition, the EMI shielding effectiveness reaches up to 69.9â¯dB at 8.2-12.4â¯GHz. In conclusion, the synthesized PLGN composite phase change material demonstrates considerable promise for mitigating electromagnetic interference and facilitating thermal energy management in electronic devices.
RESUMO
NRF2 (NFE2L2) is a transcription factor mainly for regulating cellular antioxidant response and therefore promotes tumor progression. The target genes of NRF2 also play important roles in cellular processes including glucose metabolism, de novo serine synthesis, iron metabolism, etc. Here, by modulating NRF2 expression in lung adenocarcinoma (LUAD) cells, we showed that NRF2 regulated EGF expression at protein level. Furthermore, EGF was identified as a ubiquitinated protein. We predicted three deubiquitinases of EGF, and OTUD4 had the highest correlation with NRF2 in LUAD among the three. OTUD4 expression was reduced upon NRF2 knocking-down and recovered upon NRF2 rescuing in A549 cells. Then a potential binding site for NRF2 in OTUD4 promoter was searched out. By binding with OTUD4 promoter, NRF2 transcriptionally activated OTUD4, thus promoted EGF deubiquitination and enhanced its stability. More importantly, OTUD4 and NRF2 expression was found being correlated in LUAD patients. The data collectively revealed a novel mechanism of NRF2 regulating on EGF stability through OTUD4 in LUAD.
Assuntos
Adenocarcinoma de Pulmão , Neoplasias Pulmonares , Humanos , Adenocarcinoma de Pulmão/genética , Fator de Crescimento Epidérmico/metabolismo , Regulação da Expressão Gênica , Neoplasias Pulmonares/genética , Fator 2 Relacionado a NF-E2/genética , Fator 2 Relacionado a NF-E2/metabolismo , Proteases Específicas de Ubiquitina/metabolismoRESUMO
Ferroptosis is an iron-dependent and lipid peroxidation-driven cell death cascade, occurring when there is an imbalance of redox homeostasis in the cell. Nuclear factor erythroid 2-related factor 2 (NFE2L2, also known as NRF2) is key for cellular antioxidant responses, which promotes downstream genes transcription by binding to their antioxidant response elements (AREs). Numerous studies suggest that NRF2 assumes an extremely important role in the regulation of ferroptosis, for its various functions in iron, lipid, and amino acid metabolism, and so on. Many pathological states are relevant to ferroptosis. Abnormal suppression of ferroptosis is found in many cases of cancer, promoting their progression and metastasis. While during tissue damages, ferroptosis is recurrently promoted, resulting in a large number of cell deaths and even dysfunctions of the corresponding organs. Therefore, targeting NRF2-related signaling pathways, to induce or inhibit ferroptosis, has become a great potential therapy for combating cancers, as well as preventing neurodegenerative and ischemic diseases. In this review, a brief overview of the research process of ferroptosis over the past decade will be presented. In particular, the mechanisms of ferroptosis and a focus on the regulation of ferroptosis by NRF2 will be discussed. Finally, the review will briefly list some clinical applications of targeting the NRF2 signaling pathway in the treatment of diseases.