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Voltage-dependent anion channel 1 (VDAC1) is a pore protein located in the outer mitochondrial membrane. Its channel gating mediates mitochondrial respiration and cell metabolism, and it has been identified as a critical modulator of mitochondria-mediated apoptosis. In many diseases characterized by mitochondrial dysfunction, such as cancer and neurodegenerative diseases, VDAC1 is considered a promising potential therapeutic target. However, there is limited research on the regulatory factors involved in VDAC1 protein expression in both normal and pathological states. In this study, we find that VDAC1 protein expression is up-regulated in various neuronal cell lines in response to intracellular metabolic and oxidative stress. We further demonstrate that VDAC1 expression is modulated by intracellular ATP level. Through the use of pharmacological agonists and inhibitors and small interfering RNA (siRNA), we reveal that the AMPK/PGC-1α signaling pathway is involved in regulating VDAC1 expression. Additionally, based on bioinformatics predictions and biochemical verification, we identify p53 as a potential transcription factor that regulates VDAC1 promoter activity during metabolic oxidative stress. Our findings suggest that VDAC1 expression is regulated by the AMPK/PGC-1α and p53 pathways, which contributes to the maintenance of stress adaptation and apoptotic homeostasis in neuronal cells.

In the electrocatalytic CO2 reduction reaction (CO2RR), metal catalysts with an oxidation state generally demonstrate more favorable catalytic activity and selectivity than their corresponding metallic counterparts. However, the persistence of oxidative metal sites under reductive potentials is challenging since the transition to metallic states inevitably leads to catalytic degradation. Herein, a thorough review of research on oxidation-state stabilization in the CO2RR is presented, starting from fundamental concepts and highlighting the importance of oxidation state stabilization while revealing the relevance of dynamic oxidation states in product distribution. Subsequently, the functional mechanisms of various oxidation-state protection strategies are explained in detail, and in situ detection techniques are discussed. Finally, the prevailing and prospective challenges associated with oxidation-state protection research are discussed, identifying innovative opportunities for mechanistic insights, technology upgrades, and industrial platforms to enable the commercialization of the CO2RR. [ABSTRACT FROM AUTHOR]

Electrocatalytic CO2 reduction (ECR) powered by renewable electricity has attracted of wide attention because of its advantages to produce high‐value‐added chemicals and fuels. Additionally, ECR played a crucial role in addressing the challenge of excessive fossil fuel consumption caused by global warming. Herein, a unique armor structure with Ni nanoparticles coated by a carbon shell containing Ni─N─C (Ni─NP@Ni─SA) for industrial ECR to CO in pH‐universal electrolytes is designed. Ni─NP@Ni─SA catalyst exhibits ≈100% CO Faradaic efficiency, and CO partial current density can reach 500, 361, and 615 mA cm−2 in strong alkaline (pH 14), neutral (pH 7.2) and strong acidic (pH 1) electrolytes, respectively. Moreover, Ni─NP@Ni─SA can drive the rechargeable Zn‐CO2 battery with a high power density of 3.45 mW cm−2, and outstanding stability over 36 h. The structural characterizations and theoretical calculation together present that the electron penetration effect of Ni─NP@Ni─SA can strengthen the electronic enrichment state of Ni single atom, which facilitates the reaction kinetics of ECR by decreasing the formation energy barrier of key intermediate *COOH. This work pioneers a new design strategy to enhance the activity of single‐atom catalysts and seek high‐efficiency electrocatalysts for ECR in pH‐universal electrolytes. [ABSTRACT FROM AUTHOR]

Background: Compared with anti-infective drugs, immunosuppressants and other fields, the application of therapeutic drug monitoring (TDM) in oncology is somewhat limited. Objective: We aimed to provide a comprehensive understanding of TDM guidelines for antineoplastic drugs and to promote the development of individualized drug therapy in oncology. Design: This study type is a systematic review. Data sources and methods: This study was performed and reported according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 statement. Databases including PubMed, Embase, the official websites of TDM-related associations and Chinese databases were comprehensively searched up to March 2023. Two investigators independently screened the literature and extracted data. The methodological and reporting quality was evaluated using the Appraisal of Guidelines for Research and Evaluation II (AGREE II) and the Reporting Items for Practice Guidelines in Healthcare (RIGHT), respectively. Recommendations and quality evaluation results were presented by visual plots. This study was registered in PROSPERO (No. CRD42022325661). Results: A total of eight studies were included, with publication years ranging from 2014 to 2022. From the perspective of guideline development, two guidelines were developed using evidence-based methods. Among the included guidelines, four guidelines were for cytotoxic antineoplastic drugs, three for small molecule kinase inhibitors, and one for antineoplastic biosimilars. Currently available guidelines and clinical practice provided recommendations of individualized medication in oncology based on TDM, as well as influencing factors. With regard to methodological quality based on AGREE II, the average overall quality score was 55.21%. As for the reporting quality by RIGHT evaluation, the average reporting rate was 53.57%. Conclusion: From the perspective of current guidelines, TDM in oncology is now being expanded from cytotoxic antineoplastic drugs to newer targeted treatments. Whereas, the types of antineoplastic drugs involved are still small, and there is still room for quality improvement. Furthermore, the reflected gaps warrant future studies into the exposure–response relationships and population pharmacokinetics models. [ABSTRACT FROM AUTHOR]

Coprophagy prevention (CP) affects the growth performance, hepatic lipid synthesis, and gut microbiota in rabbits. Supplementation with Clostridium butyricum (C. butyricum, Strain number: CCTCC M 2019962) has been found to improve growth performance in rabbits. However, it remains unknown whether C. butyricum can ameliorate the effects of CP on hepatic lipid synthesis and the underlying mechanisms are yet to be elucidated. Therefore, this study aimed to investigate the impact of CP on hepatic lipid synthesis and the underlying mechanism based on the gut–liver axis. The findings revealed that supplementation with C. butyricum could reverse CP-related growth performance, lipid accumulation, bile acid synthesis, and inflammation. Furthermore, C. butyricum exerted protective effects on the gut by preserving intestinal barrier integrity and modulating gut microbiota composition; these factors may represent potential mechanisms through which C. butyricum improves CP-related outcomes. Specifically, C. butyricum reshaped the microbiota by increasing butyric acid levels, thereby maintaining secondary bile acid (deoxycholic acid, chenodeoxycholic acid) balance and attenuating the inhibitory effects of the FXR/SHP pathway on lipid synthesis (SREBP1c/ApoA1). Moreover, the activation of butyrate/GPR43pathway by C. butyricum reduced damage to the intestinal barrier (ZO-1/Occludin/Claudin1) and restored the gut immune microenvironment in CP rabbits. In summary, supplementation with C. butyricum can alleviate the adverse effects of CP on growth performance and hepatic lipid synthesis by modulating the gut–liver axis. [ABSTRACT FROM AUTHOR]