Activation Pathway Research Articles

Platelet-derived extracellular vesicles induced through different activation pathways drive melanoma progression by functional and transcriptional changes

BackgroundBeyond their conventional roles in hemostasis and wound healing, platelets have been shown to facilitate hematogenous metastasis by interacting with cancer cells. Depending on the activation route, platelets also generate different platelet-derived extracellular vesicles (PEVs) that may educate cancer cells in the circulation or within the tumor microenvironment. We engaged different platelet-activating receptors, including glycoprotein VI and C-type lectin-like receptor 2, to generate a spectrum of PEV types. This allowed us to investigate the differential capacity of PEVs to alter cancer hallmark functions such as proliferation, invasion, and pro-angiogenic potential using melanoma as a model. Additionally, we analyzed changes in the cell transcriptomes and cancer EV profiles.MethodsTwo human melanoma cell lines (MV3 and A2058) with differential metastatic potential were studied in the 3D spheroid cultures. Human platelets were activated with collagen related peptide (CRP), fucoidan from Fucus vesiculosus (FFV), thrombin & collagen co-stimulus and Ca2+ ionophore, and PEVs were isolated by size-exclusion chromatography followed by ultrafiltration. Spheroids or cells were treated with PEVs and used in functional assays of proliferation, invasion, and endothelial tube formation as well as for the analysis of cancer EV production and their tetraspanin profiles. Differentially expressed genes and enriched signaling pathways in the PEV-treated spheroids were analyzed at 6 h and 24 h by RNA sequencing.ResultsAmong the studied PEVs, those generated by CRP and FFV exhibited the most pronounced effects on altering cancer hallmark functions. Specifically, CRP and FFV PEVs increased proliferation in both MV3 and A2058 spheroids. Distinct tetraspanin signatures of melanoma EVs were induced by all PEV types. While the PI3K-Akt and MAPK signaling pathways were activated by both CRP and FFV PEVs, they differently upregulated the immunomodulatory TGF-β and type-I interferon signaling pathways, respectively.ConclusionsOur study revealed both shared and distinct, cancer-promoting functions of PEVs, which contributed to the transcriptome and metastatic capabilities of the melanoma spheroids. Inhibiting the platelet receptors that modulate the PEVs’ cancer-promoting properties may open up new strategies for identifying promising treatment targets for cancer therapy.

Fischer-Speier Esterification and Beyond: Recent Mechanicistic Advances

Over the past 130 years, Fischer-Speier esterification has been established as the benchmark method for synthesizing esters from organic acids and alcohols. The reaction’s versatility, arising from the vast combinations of starting materials and the numerous catalytic alternatives to the traditional H2SO4, has maintained its relevance, with a steady flow of publications addressing new developments. This review highlights the most significant contributions to Fischer-Speier esterification over the past five years, with a particular emphasis on mechanistic advancements and innovative catalytic systems. Both homogeneous and heterogeneous catalytic approaches are discussed, including novel catalysts leveraging hydrogen-bonding interactions and systems offering fresh insights into specific reaction mechanisms and atypical methodologies. Some of these catalytic systems, as ionic liquids or sulfonated heterogeneous catalytic precursors, reached excellent yields (>90%), e.g., in the synthesis of fatty acids methyl esters. Also, classic catalysts such as H2SO4 and para-toluen sulfonic acid were optimized for quantitative conversions (e.g., in the esterification of trans-cinnamic acid with methanol). A consistent number of catalysts was studied with model substrates (as benzoic acid in combination with methanol, ethanol, and ethylene glycol), and new activation pathways were presented.

Identifying the key role of mitochondrial respiration and lipid metabolism in regulating axillary osmidrosis through proteomics analysis.

Axillary osmidrosis (AO) affects a large number of young people in Asia, resulting from a combination of body and bacterial metabolism. This study aimed to explore the pathogenesis of AO through proteomics. Apocrine gland tissues from 3 mild and 3 severe AO patients were analyzed using 4D label-free proteomics, followed by bioinformatics analysis. The RNA and protein levels of the predicted key regulators were further validated by qPCR and immunohistochemistry in additional AO tissues. A total of 5066 proteins were identified, of which 323 were significantly upregulated and 412 were downregulated (by |log2FC|> 1 and p < 0.05). GO terms related to mitochondria, oxidation-reduction processes, and peroxisomes were significantly enriched among the upregulated DEPs, suggesting enhanced energy metabolism in severe AO patients. Downregulated DEPs were enriched in ribosome, phagosome, and platelet activation pathways according to KEGG, while upregulated DEPs were significantly enriched in metabolic pathways, valine, leucine, and isoleucine degradation, peroxisomes, and fatty acid degradation. The enriched pathways suggest that apocrine gland tissues develop AO by increasing blood flow to promote sweating and secreting excessive short-chain fatty acids by coupling mitochondrial respiration with incomplete metabolism of lipids and branched-chain amino acids. This metabolic coupling may have implications for studies on cardiovascular disease, metabolic disorders, and oxidative stress. Key proteins in the signaling network were further confirmed by qPCR and immunohistochemistry, including reduced FGA and ITGA2B, and increased EHHADH and ACOX1. Our proteomics analysis suggests a paradigm of lipid metabolism involving mitochondrial respiration and incomplete lipid and branched-chain amino acid metabolism as the pathogenesis of AO. We also suggest that EHHADH is a key regulator in promoting AO in this process.

Circuits and mechanisms for TMS-induced corticospinal waves: Connecting sensitivity analysis to the network graph.

Transcranial magnetic stimulation (TMS) is a non-invasive, FDA-cleared treatment for neuropsychiatric disorders with broad potential for new applications, but the neural circuits that are engaged during TMS are still poorly understood. Recordings of neural activity from the corticospinal tract provide a direct readout of the response of motor cortex to TMS, and therefore a new opportunity to model neural circuit dynamics. The study goal was to use epidural recordings from the cervical spine of human subjects to develop a computational model of a motor cortical macrocolumn through which the mechanisms underlying the response to TMS, including direct and indirect waves, could be investigated. An in-depth sensitivity analysis was conducted to identify important pathways, and machine learning was used to identify common circuit features among these pathways. Sensitivity analysis identified neuron types that preferentially contributed to single corticospinal waves. Single wave preference could be predicted using the average connection probability of all possible paths between the activated neuron type and L5 pyramidal tract neurons (PTNs). For these activations, the total conduction delay of the shortest path to L5 PTNs determined the latency of the corticospinal wave. Finally, there were multiple neuron type activations that could preferentially modulate a particular corticospinal wave. The results support the hypothesis that different pathways of circuit activation contribute to different corticospinal waves with participation of both excitatory and inhibitory neurons. Moreover, activation of both afferents to the motor cortex as well as specific neuron types within the motor cortex initiated different I-waves, and the results were interpreted to propose the cortical origins of afferents that may give rise to certain I-waves. The methodology provides a workflow for performing computationally tractable sensitivity analyses on complex models and relating the results to the network structure to both identify and understand mechanisms underlying the response to acute stimulation.

Fuel‐Driven π‐Conjugated Superstructures to Form Transient Conductive Hydrogels

AbstractDespite advances in creating dissipative materials with transient properties, such as hydrogels and active droplets, their application remains confined to temporal changes in structural properties. Developing out‐of‐equilibrium materials whose electronic functions are parameterized by a chemical reaction cycle is challenging. Yet, this class of materials is required to construct biomimetic materials. In contrast to traditional chemical reaction cycles that exploit molecularly dissolved building blocks at thermodynamic equilibrium, we show that fiber structures derived from reactive naphthalene diimide (NDI) building blocks can be used as resting states to form far‐from‐equilibrium conductive hydrogels after the addition of chemical fuels. Upon fueling the NDI‐derived fibers, a dual‐component activation and deactivation pathway is deduced by kinetic analysis and is absent when using a molecularly dissolved resting state. Investigating the solid‐state morphologies of the structures formed throughout the fuel‐driven reaction cycle using cryo‐EM reveals that the resting thermodynamic fibers evolve to transient thicker fibrils and layered superstructures. We show that the transient redox‐active hydrogels exhibit a nearly threefold increase in electrical conductivity upon fuel consumption before reverting to their original value over hours. These far‐from‐equilibrium materials are potential candidates in applications such as programmable biorobotics and chemical computing.

Variation in HIV-1 Tat activity is a key determinant in the establishment of latent infection.

Despite effective treatment, Human immunodeficiency virus (HIV) persists in optimally treated people as a transcriptionally silent provirus. Latently infected cells evade the immune system and the harmful effects of the virus, thereby creating a long-lasting reservoir of HIV. To gain a deeper insight into the molecular mechanisms of HIV latency establishment, we constructed a series of HIV-1 fluorescent reporter viruses that distinguish active versus latent infection. We unexpectedly observed that the proportion of active-to-latent infection depended on a limiting viral factor, which created a bottle neck that could be overcome by superinfection of the cell, T cell activation or overexpression of HIV-1 trans activator of transcription (Tat). In addition, we found that tat and rev expression levels vary amongst HIV molecular clones and that tat levels were an important variable in latency establishment. Lower rev levels limited viral protein expression whereas lower Tat levels or mutation of the Tat binding element promoted latent infection that was resistant to reactivation even in fully activated primary T cells. Nevertheless, we found that combinations of latency reversal agents targeting both cellular activation and histone acetylation pathways overcame deficiencies in the Tat-TAR axis of transcription regulation. These results provide additional insight into the mechanisms of latency establishment and inform Tat-centered approaches to cure HIV.

Gene expression profiling of indigenous Tharparkar and crossbred Vrindavani cattle affected with lameness using PBMC model.

Lameness is an economically significant, production-limiting syndrome that adversely affects the (re)production performance of animals besides deteriorating the quantity and quality aspects of milk in dairy cattle. The present study aimed to explore the potential biomarkers for painful foot lesions in indigenous Tharparkar and crossbredVrindavani cattle affected with lameness. The differentially expressed genes in lame versus healthy animals were elucidated using microarray analysis and validated them by qRT-PCR. On microarray analysis, 504 genes were differentially expressed in lame crossbred cattle as compared to healthy counterparts. Similarly, 991 genes were differentially expressed in lame crossbred cattle as compared to the healthy Tharparkar animals. Various genes such as BOLA-DQA3, BOLA-DQA1, CCL4, CCR1, CCRL2, CXCL2, CXCL3, CXCL8, IL1A, IL1B, MMP-9 and SLC11A1 were common between both the comparisons (crossbred lame vs. crossbred normal cattle; and crossbred lame vs. normal Tharparkar cattle). The results revealed downregulation of multiple pro-inflammatory cytokines. Validation using qRT-PCR showed high correlation with the microarray results, except for the IRAK1 gene. The functional annotation and gene network analysis revealed involvement of various processes including inflammation, immunology, apoptosis, cell proliferation and cytoskeleton organization. The Ingenuity pathway analysis revealed three inhibited pathways in the comparison between lame and normal (healthy) crossbred cattle i.e., HMGB1-signalling pathway, Aryl hydrocarbon receptor signalling pathway, and Mitotic roles of pol-like kinase. Whereas, on comparison of lame crossbred with healthy Tharparkar cattle, the Situin signalling pathway was inhibited; the LxR/RxR activation pathway was activated. The results from microarray analysis, identifying differential expressed genes provides valuable insights into the development of molecular biomarkers for early detection of lameness-affected animals.

Complement factor B, not the membrane attack complex component C9, promotes neointima formation after arterial wire injury

Background and aimsVascular restenosis due to neointima hyperplasia limits the long-term patency of stented arteries, resulting in angioplasty failure. The complement system has been implicated in restenosis. This study aimed to investigate the role of complement factor B (fB), an essential component of the alternative pathway of complement activation, in neointima formation. MethodsAngioplasty wire injury was conducted using 12-week-old mice deficient in fB or C9 (the main component of the membrane attacking complex, C5b-9) and littermate controls and neointima formation were assessed. Vascular smooth muscle cell (SMC) and endothelial cell (EC) proliferation and migration were examined in vitro. ResultsfB was mainly detected in SMCs of stenotic arteries from humans and mice. Deletion of fB substantially reduced the neointima area and intima-to-media area ratio without affecting the media area at 28 days after injury. At 7 days after injury, fB deficiency decreased SMC proliferation, unaltering neointimal macrophage infiltration and EC reendothelialization. Vascular SMC-expressed fB, not the circulation-sourced fB, played an essential role in SMC proliferation and migration in vitro. fB deficient mice exhibited lower levels of the soluble form of C5b-9, however, deletion of C9 did not alter neointima formation after wire injury, consistent with the null impact of C9 deficiency on SMC proliferation in vitro. ConclusionfB promotes neointima formation following wire-induced artery injury independent of forming the membrane-attacking complex. This is attributable to fB-dependent SMC proliferation and migration without affecting EC function. Targeting fB might protect against restenosis after percutaneous coronary intervention.

Adenoviral-vectored neoantigen vaccine augments hyperexpanded CD8+ T cell control of tumor challenge in mice

BackgroundNeoantigens are promising immunogens for cancer vaccines and are often delivered as adjuvanted peptide vaccines. Adenoviral (Ad) vectors have been shown to induce strong CD8+ T cell responses as vaccines...

The Role of the Complement System in Autoimmune Diseases and Therapeutic Targeting

The complement system, a critical component of the innate immune system, plays a dual role in immune defense and pathogenesis, particularly in autoimmune diseases. Comprising over 30 proteins, the complement system facilitates pathogen clearance, inflammation, and immune modulation. However, its dysregulation can lead to uncontrolled activation and contribute to the development and progression of various autoimmune disorders, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), multiple sclerosis (MS), antiphospholipid syndrome (APS), and vasculitis. In these diseases, excessive complement activation triggers inflammation, immune cell recruitment, and tissue damage, exacerbating the autoimmune response. This review provides an in-depth analysis of the complement system’s role in autoimmune diseases, exploring how its three activation pathways—classical, lectin, and alternative—contribute to disease pathogenesis. It also discusses key complement proteins such as C3, C5, and the membrane attack complex (MAC) in promoting inflammatory responses in these conditions. Moreover, the review highlights recent advances in therapeutic strategies targeting the complement system, including the development of C5 inhibitors like eculizumab and C3 inhibitors, which show promise in treating complement-mediated autoimmune diseases. These therapies aim to reduce inflammation and tissue destruction, offering new approaches for managing autoimmune disorders. Understanding complement dysregulation is crucial for the development of more effective treatments in the future. Keywords: Complement system, Autoimmune diseases, Complement activation, Inflammation, Therapeutic targeting

C-Type Lectin S Group TcCTL4 Participates in the Immunity of Tribolium castaneum.

C-type lectin S (CTL-S) plays a crucial role in pathogen recognition and the activation of immune response. In comparison, the proportion of CTL-S was relatively high in insects, but the study was much smaller than the proportion observed. In this study, we cloned and characterized one CTL-S, TcCTL4, from Tribolium castaneum. Our analysis revealed that TcCTL4 was highly expressed during the early pupal stage, with expression levels exhibiting a tendency to change with developmental stages. Additionally, tissue expression analysis showed a high expression of TcCTL4 in the central nervous system (CNS). Moreover, we observed a significant increase in TcCTL4 transcripts after bacterial challenge. The RNA interference (RNAi) of TcCTL4 before bacterial treatment resulted in a significant reduction in the transcripts of immune factors (IFs) and antimicrobial peptides (AMPs), indicating that TcCTL4 may regulate AMP expression through the activation of the immune signaling pathway. Furthermore, our investigation revealed that the recombinant protein TcCTL4 (rTcCTL4) not only recognized bacteria but also agglutinated bacteria in a Ca2+-dependent manner. Enzyme activity analysis suggested that rTcCTL4 could enhance phenoloxidase activity, implying its potential involvement in the prophenoloxidase activation pathway. In conclusion, these results indicate that TcCTL4 is involved in the immunity of T. castaneum, providing valuable insights into insect CTLs.

Molecular Mechanisms Underlying Initiation and Activation of Autophagy

Autophagy is an important catabolic process to maintain cellular homeostasis and antagonize cellular stresses. The initiation and activation are two of the most important aspects of the autophagic process. This review focuses on mechanisms underlying autophagy initiation and activation and signaling pathways regulating the activation of autophagy found in recent years. These findings include autophagy initiation by liquid–liquid phase separation (LLPS), autophagy initiation in the endoplasmic reticulum (ER) and Golgi apparatus, and the signaling pathways mediated by the ULK1 complex, the mTOR complex, the AMPK complex, and the PI3KC3 complex. Through the review, we attempt to present current research progress in autophagy regulation and forward our understanding of the regulatory mechanisms and signaling pathways of autophagy initiation and activation.

Investigation of TSRP reverses imatinib resistance through the PI3K / Akt pathway in chronic myeloid leukemia.

Chronic myelogenous leukemia (CML) is a malignant tumor of the blood system, so far there is no effective cure. Imatinib (IM), as the first-line drug for the clinical targeted treatment of CML, has some limiting factors such as drug resistance and relapse, and drug resistance has also emerged in combination with other drugs. At present, traditional Chinese medicine combined with targeted drugs in the treatment of tumor is a research hotspot. The total saponin of L. (TSRP) has an effective anti-tumor activity. Our previous in vitro experiments showed that TSRP can effectively inhibit the proliferation and promote apoptosis of CML cells K562, suggesting that TSRP can effectively reverse the drug resistance of IM, but the mechanism of drug resistance remains unclear. Studies have shown that the PI3K/AKT pathway is the main activation pathway of IM secondary resistance, and is considered to be an innovative therapeutic strategy for targeted cancer treatment, which may be an important mechanism of IM resistance. This project aims to reveal the possible mechanism of TSRP reversing IM resistance through PI3K/AKT signaling pathway through both in vitro and in vivo experiments, providing experimental basis for TSRP combined with IM treatment of CML.

Treatment advances of sepsis‑induced myopathy (Review).

Sepsis-induced myopathy (SIM) is a muscle disease caused by multiple pathological and physiological mechanisms associated with sepsis. The pathogenesis of SIM is extremely complex and still unclear, making treatment challenging. At present, clinical treatment includes early functional exercise, respiratory muscle strength training, regulation of nutritional structure and functional electrical stimulation. Drugs targeting the regulation of the ubiquitin-proteasome system, autophagy-lysosome system, calpain and caspase activation pathways, have provided potential therapeutic targets for the treatment of muscle atrophy. Stem cell transplantation therapy brings new hope for the treatment of SIM.

Systemic Toxicity of Recombinant Adeno-Associated Virus Gene Therapy Vectors.

Recombinant adeno-associated virus (rAAV) vectors have emerged as a promising tool for gene therapy. However, the systemic administration of rAAV vectors is not without risks, particularly for dose levels >1 × 1014 viral genome per kilogram of body weight (vg/kg). rAAV-associated toxicities can variably manifest either acutely or in a delayed manner. Acute toxicities often present shortly after administration and can include severe immune responses, hepatotoxicity, and thrombotic microangiopathy (TMA). Delayed toxicities, on the other hand, may emerge weeks to months post-treatment, potentially involving chronic liver damage or prolonged immune activation. Thrombotic microangiopathy is often associated with complement activation and endothelial damage. The activation of the complement system can additionally trigger a cascade of inflammatory responses, exacerbating systemic toxicity. While many of these toxicities are reversible with appropriate medical intervention, there have been instances where the adverse effects were severe enough to lead to fatalities. Both human and animal studies have reported these adverse effects, highlighting the critical importance of thorough preclinical testing. However, a differential toxicity profile associated with systemic AAV administration exists between humans and nonhuman primates (NHPs), in which certain toxicities reported in humans are yet to be observed in NHPs, and vice versa. This review aims to explore the recent literature on systemic rAAV toxicities, focusing on dose levels, the role of the complement activation pathway, endothelial injury, TMA, hepatotoxicity, and the bidirectional translational safety profiles from both human and animal studies.

Surface hydroxyls of spinel oxides: A double-edged sword in the peroxymonosulfate activation process

The sulfate-based advanced oxidation process (SR-AOP) mediated by spinel oxides has shown great potential in pollutant degradation. However, the role of surface hydroxyls in the reaction process remains unclear, especially in real environments containing salts. Here, we investigated the role of surface hydroxyls of spinel oxides in activating peroxymonosulfate (PMS). By adjusting the intrinsic composition of the metal elements, we synthesized a CoFeMnO4 spinel with high surface hydroxyls using a simple and scalable co-precipitation method. CoFeMnO4 demonstrated unparalleled activation performance and a unique non-radical activation pathway (dominated by high-valence metal-oxo species and singlet oxygen), achieving 100 % sulfamethoxazole degradation within 4 min with a low concentration of PMS. Surface hydroxyls of CoFeMnO4 played a crucial role in the activation process, serving as adsorption sites for PMS and facilitating its activation. Interestingly, we discovered that several common anions (Cl−, HCO3−, SO42− and NO3−) could undergo ligand exchange with surface hydroxyls of CoFeMnO4, occupying some of sites intended for PMS adsorption, which significantly inhibited the PMS decomposition on the catalyst surface. Further, it was finally discovered that the inhibition of the reaction system by these anions was primarily due to their competition for surface hydroxyls, rather than the commonly believed the consumption of reactive oxygen species by anions. Given the inevitable presence of various anions in real water bodies, this finding highlights the dual nature of surface hydroxyls as active sites in SR-AOPs: While they aid in activation process, the competition from anions for them would diminish the overall system performance.

Single-Cell Transcriptomics of Human Tonsils Reveals Nicotine Enhances HIV-1-Induced NLRP3 Inflammasome and Mitochondrial Activation.

HIV-1 infection, even with effective antiretroviral therapy (ART), is associated with chronic inflammation and immune dysfunction, contributing to long-term health complications. Nicotine use, prevalent among people with HIV (PWH), is known to exacerbate immune activation and disease progression, but the precise biological mechanisms remain to be fully understood. This study sought to uncover the synergistic effects of HIV-1 infection and nicotine on immune cell function, focusing on beneficial insights into NLRP3 inflammasome activation, oxidative stress, and mitochondrial pathways. Human tonsil explants were infected with HIV-1 and exposed to nicotine. Single-cell RNA sequencing was used to profile immune cell populations and gene expression linked to inflammasome activation, oxidative stress, and mitochondrial function. Gene set enrichment analysis (GSEA) and synergy assessments were conducted to investigate how nicotine modulates immune responses in the context of HIV. The combination of HIV infection and nicotine exposure significantly increased NLRP3 inflammasome activation, thioredoxin, and components of oxidative phosphorylation. This study highlights how the combined effects of HIV-1 and nicotine offer valuable insights into immune modulation, opening doors for future therapeutic strategies. Targeting the NLRP3 inflammasome and addressing nicotine use may contribute to improved outcomes for PWH.

Combined Mendelian randomization and quantitative proteomics analysis to study the influence of thyroid dysfunction on acute ischemic stroke

AbstractAcute ischemic stroke (AIS) is characterized by high morbidity and mortality, making it crucial to identify the risk factors that influence its occurrence and prognosis. Although individuals with thyroid dysfunction exhibit altered stroke patterns, evidence from observational studies remains inconsistent. Herein, we investigated the influence of thyroid dysfunction on stroke progression and prognosis. We combined Mendelian randomization (MR) and tandem mass tag (TMT)‐based quantitative proteomics analysis to study the influence of thyroid dysfunction on AIS. Differentially expression proteins (DEPs) were subsequently identified, functional enrichment analysis was performed, and a protein–protein interaction (PPI) network was constructed. Protein alterations were further validated by western blot. MR analysis revealed a causal association between thyroid disorders and ischemic stroke. DEP analysis identified 38 downregulated proteins and five upregulated proteins. Functional enrichment analysis and PPI network construction highlighted the importance of immune response activation and acute phase pathways, along with the suppression of focal adhesion, regulation of the actin cytoskeleton, and platelet activation pathways. Vasodilator‐stimulated phosphoprotein, MYL12B, MYL6, and TPM4 were identified as key DEPs significantly associated with pathological pathways and were verified by western blot. The identification of these key proteins and pathways provides new perspectives for investigating the progression and prognosis of AIS.

Oxidative Stress and Cancer Therapy: Controlling Cancer Cells Using Reactive Oxygen Species.

Cancer is a multifaceted disease influenced by various mechanisms, including the generation of reactive oxygen species (ROS), which have a paradoxical role in both promoting cancer progression and serving as targets for therapeutic interventions. At low concentrations, ROS serve as signaling agents that enhance cancer cell proliferation, migration, and resistance to drugs. However, at elevated levels, ROS induce oxidative stress, causing damage to biomolecules and leading to cell death. Cancer cells have developed mechanisms to manage ROS levels, including activating pathways such as NRF2, NF-κB, and PI3K/Akt. This review explores the relationship between ROS and cancer, focusing on cell death mechanisms like apoptosis, ferroptosis, and autophagy, highlighting the potential therapeutic strategies that exploit ROS to target cancer cells.

Aeration‐Free Photo‐Fenton‐Like Reaction Mediated by Heterojunction Photocatalyst toward Efficient Degradation of Organic Pollutants

The regulation of peroxymonosulfate (PMS) activation by photo‐assisted heterogeneous catalysis is under in‐depth investigation with potential as a replaceable advanced oxidation process in water purification, yet it remains a significant challenge. Herein, we demonstrate a strategy to construct polyethylene glycol (PEG) well‐coupled dual‐defect VO‐M‐Co3O4@CNx S‐scheme heterojunction to degrade organic pollutants without aeration, which dramatically provides abundant active sites, excellent photo‐thermal property, and distinct charge transport pathway for PMS activation. The degradation rate of VO‐M‐Co3O4@CNx in anaerobic conditions shows a higher efficient rate (4.58 min‐1 g‐2) than in aerobic conditions (1.67 min‐1 g‐2). Experimental evidence reveals that VO‐M‐Co3O4@CNx promotes more rapid redox conversion of photoexcited electrons induced by defects with PMS under anaerobic conditions compared to aerobic conditions. Additionally, in situ experiments and DFT provide mechanistic insights into the regulation pathway of PMS activation via synergistic defect‐induced electron, revealing the competitive effect between O2 and PMS over VO‐M‐Co3O4@CNx during the reaction process. The continuous flow reactor and flow cytometry results demonstrated that the VO‐M‐Co3O4@CNx/PMS/Vis system has remarkably enhanced stability and purification capability for removing organic pollutants. This work provides valuable insights into regulating the heterologous catalysis oxidation process without aeration through the photoexcitation synergistic PMS activation.