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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is continuously producing new variants, necessitating effective therapeutics. Patients are not only confronted by the immediate symptoms of infection but also by the long-term health issues linked to long COVID-19. Activation of epidermal growth factor receptor (EGFR) signalling during SARS-CoV-2 infection promotes virus propagation, mucus hyperproduction, and pulmonary fibrosis, and suppresses the host's antiviral response. Over the long term, EGFR activation in COVID-19, particularly in COVID-19-induced pulmonary fibrosis, may be linked to the development of lung cancer. In this review, we have summarised the significance of EGFR signalling in the context of SARS-CoV-2 infection. We also discussed the targeting of EGFR signalling as a promising strategy for COVID-19 treatment and highlighted erlotinib as a superior option among EGFR inhibitors. Erlotinib effectively blocks EGFR and AAK1, thereby preventing SARS-CoV-2 replication, reducing mucus hyperproduction, TNF-α expression, and enhancing the host's antiviral response. Nevertheless, to evaluate the antiviral efficacy of erlotinib, relevant clinical trials involving an appropriate patient population should be designed.

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Tobacco has a strong cadmium (Cd) enrichment capacity, meaning that it can absorb large quantities from the environment, but too much Cd will cause damage to the plant. It is not yet clear how the plant can dynamically respond to Cd stress. Here, we performed a temporal transcriptome analysis of tobacco roots under Cd treatment from 0 to 48 h. The number of differentially expressed genes (DEGs) was found to change significantly at 3 h of Cd treatment, which we used to define the early and middle stages of the Cd stress response. The gene ontology (GO) term analysis indicates that genes related to photosynthesis and fatty acid synthesis were enriched during the early phases of the stress response, and in the middle phase biological process related to metal ion transport, DNA damage repair, and metabolism were enriched. It was also found that plants use precursor mRNA (pre-mRNA) processes to first resist Cd stress, and with the increasing of Cd treatment time, the overlapped genes number of DEGs and DAS increased, suggesting the transcriptional levels and post-transcriptional level might influence each other. This study allowed us to better understand how plants dynamically respond to cadmium stress at the transcriptional and post-transcriptional levels and provided a reference for the screening of Cd-tolerant genes in the future.

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The bZIP proteins comprise one of the largest transcription factor families and play important roles in plant growth and development, senescence, metabolic reactions, and stress responses. In this study, 49 bZIP transcription factor-encoding genes (StbZIP genes) on the potato genome were identified and analyzed. The 49 StbZIP genes, which are located on 12 chromosomes of the potato genome, were divided into 11 subgroups together with their Arabidopsis homologs based on the results of phylogenetic analysis. Gene structure and protein motif analysis revealed that members from the same subgroup often possessed similar exon/intron structures and motif organizations, further supporting the results of the phylogenetic analysis. Syntenic analysis indicated the existence of gene duplication events, which might play an important role in the expansion of the bZIP gene family in potato. Expressions of the StbZIP genes were analyzed in a variety of tissues via RNA-Seq data, suggesting functional diversity. Several StbZIP genes were found to be induced by different stress conditions. For example, the expression of StbZIP25, the close homolog of AtbZIP36/ABF2, was significantly upregulated by salt stress treatments. The StbZIP25 protein was found to be located in the nucleus and function as a transcriptional activator. Overexpression of StbZIP25 enhanced salt tolerance in Arabidopsis. The results from this study imply potential roles of the bZIP family genes in the stress response of potato.

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Cigarette smoking, as an individual consumption habit, is associated with a variety of related diseases. Exposure of cigarette smoke was reported to induce autophagy and inflammation in experimental animals and humans. However, the toxicity mechanism of cigarette smoke in organisms has not been entirely investigated. In this present study, we studied the role of autophagy played in the inflammation caused by cigarette smoke in human bronchial epithelial cells (BEAS-2B), as well as the role of the phosphatidylinositol 3-kinase (PI3K) signaling pathway and the mitogen-activated protein kinase (MAPK) signaling pathways underlying autophagy and inflammation. We found that cigarette smoke induced autophagy and inflammation in BEAS-2B, and the blockage of autophagy significantly reduced the release levels of IL-1ß, IL-6 and IL-8 in BEAS-2B exposed to cigarette smoke for 24 h. Cigarette smoke downregulated the activity of PI3K/Akt/mTOR pathway and elevated the activity of MAPK pathways. Pretreatment of autophagic inhibitor could inhibit autophagy and the activity of JNK and p38 pathways. These results suggested that cigarette smoke-induced autophagy triggered inflammation through the activation of JNK and p38 pathways, which might contribute to understanding the adverse outcome pathways induced by cigarette smoke exposure and provide the information about the risk assessment of tobacco products.

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In this study, we employed multiple spectroscopic methods to analyze the effects of carbon nanoparticles (CNPs) on structure of cytochrome c (Cyt c) and mitochondrial function in plant cells. The tertiary structures of aromatic amino acid in Cyt c were not changed after addition of CNPs. Cyt c was found to be absorbed on the surfaces of CNPs in a non-linear manner and only bound Cyt c can be reduced. In addition, the binding of Cyt c was found to increase the diameter of CNPs at lower concentrations. The redox potential of Cyt c was almost not affected after treatment with CNPs. There were no obvious differences in cellular ATP after exposure to CNPs, and the mitochondrial membrane potential (MMP) was significantly decreased once the CNPs concentration exceeded 31.25 µg/mL. The levels of reactive oxygen species (ROS) also were increased in BY-2 cells. Taken together, these findings provide basis for the interactions between CNPs and Cyt c, as well as the effect of CNPs treatment on the mitochondria function in plant cells.

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The tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is classified as a Group 1 human carcinogen. It is metabolically activated by P450 enzymes to intermediate methylate and pyridyloxobutylate DNA, resulting in the formation of DNA adduct that is critical for the carcinogenicity of NNK. To directly and objectively examine the DNA adduct formation profiles without the complexity of factors in vivo, in the present study, five kinds of methyl DNA adducts were first identified in the incubation model of NNK established with human lung epithelial cells (BEAS-2B). The level of methyl DNA adducts and metabolites of NNK were quantitatively analyzed, respectively. With the increase of exposure time and dose, the level of methyl DNA adducts and metabolites increased. Furthermore, with the changes of the activity of P450 enzymes, which is the main enzyme regulating the α-hydroxylation of NNK, we found the levels of both methyl adducts and metabolites formed via α-hydroxylation in experimental groups showed the same trend compared with those in control group, while the metabolites formed via other pathways changed in the opposite trend. The result proves that the methyl adducts induced by NNK generate via α-hydroxylation pathway in BEAS-2B cells.

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