Effects of residual feed intake on the economic traits of fast-growing meat ducks.

Feed efficiency (FE) is a crucial economic indicator of meat duck production. The objective of this study was to assess the impact of residual feed intake (RFI), defined as the difference between the actual and expected feed intake based on animal's production and maintenance requirements, on the growth performance (GP), slaughter and internal organ characteristics of fast-growing meat ducks. In total, 1,300 healthy 14-day-old male fast-growing meat ducks were housed in individual cages until slaughter at the age of 35 d. The characteristics of the carcass and internal organs of 30 ducks with the highest RFI (HRFI) and the lowest RFI (LRFI) were respectively determined. RFI, the feed conversion ratio (FCR), and average day feed intake (ADFI) were significantly lower in the LRFI group than the HRFI group (P < 0.001), while there were no significant differences in marketing BW or BW gain (BWG) (P > 0.05). The thigh muscle and lean meat yields were higher, and the abdominal fat content was lower (P < 0.001) in the LRFI group, while there were no significant differences in other carcass traits between the groups (P > 0.05). The liver and gizzard yields were significantly higher (P < 0.001) in the LRFI group, while there were no significant differences (P > 0.05) in intestinal length between the groups. RFI was highly positively correlate with FCR and ADFI (P < 0.01), but negatively correlated the yields of thigh muscle, lean meat, liver, and gizzard, and positively correlated with abdominal fat content. These results indicate that selection for low RFI could improve the FE of fast-growing meat ducks without affecting the marketing BW and BWG, while increasing yields of thigh muscle and lean meat and reducing abdominal fat content. These findings offer useful insights into the biological processes that influence FE of fast-growing meat ducks.

Platelet PD-L1 inhibits storage-induced apoptosis by sustaining activation of the AKT signalling pathway.

Platelet apoptosis is irreversible under current storage conditions in blood banks. Studies have shown that programmed cell death ligand 1 (PD-L1) in tumour cells is required for neoplastic progression, tumour recurrence and metastasis by regulating apoptosis. However, whether PD-L1 is involved in storage-induced apoptosis in platelets remains poorly understood. In this study, we explored whether PD-L1 on platelets participated in the regulation of storage-induced apoptosis under blood bank conditions, as well as the underlying mechanism. Several apoptotic events in platelets from humans and PD-L1-knockout mice during storage under blood bank conditions were measured. The mechanism by which storage-induced apoptosis was regulated by platelet-intrinsic PD-L1 signalling was further investigated. Our results showed that PD-L1 in platelets progressively decreased. There was a strong negative correlation between platelet PD-L1 expression and the phosphatidylserine (PS) externalization rate and cleaved caspase-3 level and a positive correlation with anti-apoptosis protein Bcl-xl. Ex vivo, PD-L1-/- platelets stored at 22 °C showed rapid apoptosis via an intrinsic mitochondria-dependent pathway over time. Likewise, inhibiting PD-L1 signalling with BMS-1166 accelerated apoptosis by intrinsic mitochondria-dependent pathway. Coimmunoprecipitation analysis revealed that PD-L1 could bind AKT in platelets, and the binding capacity of both showed a progressive decrease with time. Finally, the decrease in PD-L1 expression levels during storage could be attributed to a complex process of progressive secretion. Therefore, platelet PD-L1 inhibits storage-induced apoptosis by sustaining activation of the AKT signalling pathway, which is expected to become a target for alleviating platelet storage lesions (PSLs) under current blood bank conditions.

Superior Li+ Kinetics by "Low-Activity-Solvent" Engineering for Stable Lithium Metal Batteries.

The structure of solvated Li+ has a significant influence on the electrolyte/electrode interphase (EEI) components and desolvation energy barrier, which are two key factors in determining the Li+ diffusion kinetics in lithium metal batteries. Herein, the "solvent activity" concept is proposed to quantitatively describe the correlation between the electrolyte elements and the structure of solvated Li+. Through fitting the correlation of the electrode potential and solvent concentration, we suggest a "low-activity-solvent" electrolyte (LASE) system for deriving a stable inorganic-rich EEI. Nano LiF particles, as a model, were used to capture free solvent molecules for the formation of a LASE system. This advanced LASE not only exhibits outstanding antidendrite growth behavior but also delivers an impressive performance in Li/LiNi0.8Co0.1Mn0.1O2 cells (a capacity of 169 mAh g-1 after 250 cycles at 0.5 C).

Research advances on microplastics contamination in terrestrial geoenvironment: A review.

The contamination of microplastics in terrestrial geoenvironment (CMTG) is widespread and severe and has, received considerable attention. However, studies on CMTG are in their initial stages. The literature on CMTG published in the past decade was analyzed through bibliometric analysis, such as the annual publications, countries with the highest contributions, prolific authors, and author keywords. The sources, compositions, migrations and environmental impacts of CMTG are summarized, and possible future directions are proposed. This study analyzed the annual publications, countries with the highest contributions, prolific authors, and author keywords related to microplastics. The results demonstrated that 15,306 articles were published between 2014 and 2023. China is the leading country in terms of the total number of publications. The main sources of CMTG include landfills, agricultural non-point sources, sewage treatment systems and transportation systems. The composition of the CMTG exhibits significantly temporal and spatial variability from different sources. The migration paths of the CMTG were within the soil, groundwater seepage and wind transportation of suspended particles. Microplastics increase soil cohesion, decrease porosity, reduce pore scale, decrease air circulation, and increase water retention capacity, and the exudation of highly water-soluble additives in microplastics can cause secondary contamination of geological entities. Microplastics have an adverse effect on plant growth, animal digestion, microbial activity, energy and lipid metabolism, oxidative stress, and respiratory diseases in humans. It is recommended to develop more efficient and convenient quantitative testing methods for microplastics, formulate globally harmonized testing and evaluation standards, include microplastic testing in testing programs for contaminated soils, and develop efficient methods for the remediation of microplastic contaminated geological bodies.

A novel insight into cancer therapy: Lipid metabolism in tumor-associated macrophages.

The tumor immune microenvironment (TIME) can limit the effectiveness and often leads to significant side effects of conventional cancer therapies. Consequently, there is a growing interest in identifying novel targets to enhance the efficacy of targeted cancer therapy. More research indicates that tumor-associated macrophages (TAMs), originating from peripheral blood monocytes generated from bone marrow myeloid progenitor cells, play a crucial role in the tumor microenvironment (TME) and are closely associated with resistance to traditional cancer therapies. Lipid metabolism alterations have been widely recognized as having a significant impact on tumors and their immune microenvironment. Lipids, lipid derivatives, and key substances in their metabolic pathways can influence the carcinogenesis and progression of cancer cells by modulating the phenotype, function, and activity of TAMs. Therefore, this review focuses on the reprogramming of lipid metabolism in cancer cells and their immune microenvironment, in which the TAMs are especially concentrated. Such changes impact TAMs activation and polarization, thereby affecting the tumor cell response to treatment. Furthermore, the article explores the potential of targeting the lipid metabolism of TAMs as a supplementary approach to conventional cancer therapies. It reviews and evaluates current strategies for enhancing efficacy through TAMs' lipid metabolism and proposes new lipid metabolism targets as potential synergistic options for chemo-radiotherapy and immunotherapy. These efforts aim to stimulate further research in this area.

Mechanism of non-thermal atmospheric plasma in anti-tumor: influencing intracellular RONS and regulating signaling pathways.

Non-thermal atmospheric plasma (NTAP) has been proven to be an effective anti-tumor tool, with various biological effects such as inhibiting tumor proliferation, metastasis, and promoting tumor cell apoptosis. At present, the main conclusion is that ROS and RNS are the main effector components of NTAP, but the mechanisms of which still lack systematic summary. Therefore, in this review, we first summarized the mechanism by which NTAP directly or indirectly causes an increase in intracellular RONS concentration, and the multiple pathways dysregulation (i.e. NRF2, PI3K, MAPK, NF-κB) induced by intracellular RONS. Then, we generalized the relationship between NTAP induced pathways dysregulation and the various biological effects it brought. The summary of the anti-tumor mechanism of NTAP is helpful for its further research and clinical transformation.

Non-thermal atmospheric plasma (NTAP) acts on NADPH oxidase and catalase.The feeding gas and parameters of NTAP affect its impacts on the signaling pathways.The impacts of NTAP and RONS on pathways are not always consistent.NTAP can trigger various anti-tumor biological effects.

Spermatocytes are the terminals of germ cell differentiation in plateau zokor (Eospalax baileyi) during the non-breeding season.

Plateau zokor (Eospalax baileyi) is a subterranean rodent and seasonal breeder. During the non-breeding season, the testicles regress, leading to the arrest of spermatogenesis and loss of fertility. The identification of the specific germ cell type at which spermatogenesis is arrested, as well as potential regulatory factors during the non-breeding season, is important for understanding seasonal spermatogenesis in subterranean species. This study analyzed genes in spermatocytes of plateau zokor by referring to single-cell RNA results in mice. We discovered that spermatogenesis is arrested at the spermatocyte during the non-breeding season, which was corroborated via immunofluorescence staining results. The analysis of gene expression during different stages of meiotic prophase I has revealed that germ cell development may be arrested, starting from zygonema, during the non-breeding season. Meanwhile, we discovered that the apoptosis genes were up-regulated, leading to apoptosis in spermatocytes. To confirm that the germ cell differentiation was blocked during the non-breeding season due to a decrease in the androgen level, we used androgen receptor antagonist (flutamide) to intervene in the breeding season and found that the inner diameter of the seminiferous tubules was significantly reduced, spermatogenesis was arrested, and spermatocytes underwent apoptosis. This study revealed that spermatocytes are the terminal of germ cell differentiation in plateau zokor during the non-breeding season and that the arrest of differentiation is attributed to a decline in androgen levels. Our results complement the theoretical basis of seasonal reproduction in plateau zokor.

Hopf bifurcation in an age-structured predator-prey system with Beddington-DeAngelis functional response and constant harvesting.

In this paper, an age-structured predator-prey system with Beddington-DeAngelis (B-D) type functional response, prey refuge and harvesting is investigated, where the predator fertility function f(a) and the maturation function ß ( a ) are assumed to be piecewise functions related to their maturation period τ . Firstly, we rewrite the original system as a non-densely defined abstract Cauchy problem and show the existence of solutions. In particular, we discuss the existence and uniqueness of a positive equilibrium of the system. Secondly, we consider the maturation period τ as a bifurcation parameter and show the existence of Hopf bifurcation at the positive equilibrium by applying the integrated semigroup theory and Hopf bifurcation theorem. Moreover, the direction of Hopf bifurcation and the stability of bifurcating periodic solutions are studied by applying the center manifold theorem and normal form theory. Finally, some numerical simulations are given to illustrate of the theoretical results and a brief discussion is presented.

Antimicrobial peptides in bone regeneration: mechanism and potential.

INTRODUCTION: Antimicrobial peptides (AMPs) are small-molecule peptides with a unique antimicrobial mechanism. Other notable biological activities of AMPs, including anti-inflammatory, angiogenesis, and bone formation effects, have recently received widespread attention. These remarkable bioactivities, combined with the unique antimicrobial mechanism of action of AMPs, have led to their increasingly important role in bone regeneration. AREAS COVERED: In this review, on the one hand, we aimed to summarize information about the AMPs that are currently used for bone regeneration by reviewing published literature in the PubMed database. On the other hand, we also highlight some AMPs with potential roles in bone regeneration and their possible mechanisms of action. EXPERT OPINION: The translation of AMPs to the clinic still faces many problems, but their unique antimicrobial mechanisms and other conspicuous biological activities suggest great potential. An in-depth understanding of the structure and mechanism of action of AMPs will help us to subsequently combine AMPs with different carrier systems and perform structural modifications to reduce toxicity and achieve stable release, which may be a key strategy for facilitating the translation of AMPs to the clinic.

Optimized wideband and compact multifunctional photonic device based on Sb2S3 phase change material.

In this paper, a 1 × 2 photonic switch is designed based on a silicon-on-insulator (SOI) platform combined with the phase change material (PCM), Sb2S3, assisted by the direct binary search (DBS) algorithm. The designed photonic switch exhibits an impressive operating bandwidth ranging from 1450 to 1650 nm. The device has an insertion loss (IL) from 0.44 dB to 0.70 dB (of less than 0.7 dB) and cross talk (CT) from -26 dB to -20 dB (of less than -20 dB) over an operating bandwidth of 200 nm, especially an IL of 0.52 dB and CT of -24 dB at 1550 nm. Notably, the device is highly compact, with footprints of merely 3 × 4 µm2. Furthermore, we have extended the device's functionality for multifunctional operation in the C-band that can serve as both a 1 × 2 photonic switch and a 3 dB photonic power splitter. In the photonic switch mode, the device demonstrates an IL of 0.7 dB and a CT of -13.5 dB. In addition, when operating as a 3 dB photonic power splitter, the IL is less than 0.5 dB.

Tannic acid-poloxamer self-assembled nanoparticles for advanced atherosclerosis therapy by regulation of macrophage polarization.

Atherosclerosis (AS) is a significant contributor to cardiovascular events. Advanced AS is particularly concerning, as it leads to the formation of high-risk vulnerable plaques. Current treatments for AS focus on antithrombotic and lipid-lowering interventions, which are effective in treating early-stage AS. Recent studies have shown that macrophage polarization plays a crucial role in the development of AS. This study presents a new biomedical application of natural tannic acid as an anti-inflammatory nanoplatform for advanced AS. Tannic acid-poloxamer nanoparticles (TPNP) are fabricated through self-assembly of tannic acid (TA) and poloxamer. TPNP has the potential to provide effective treatment for advanced AS. According to in vitro studies, TPNP has been found to suppress the inflammatory response in lipopolysaccharide-stimulated macrophages by scavenging reactive oxygen species (ROS), downregulating the expression levels of inflammatory cytokines (such as interleukin-10 and tumor necrosis factor-α) and regulating polarization of macrophages. In vivo studies further reveal that TPNP can retard the development of advanced atherosclerotic plaques by reducing ROS production and promoting M2 macrophage polarization in the aorta of ApoE-/- mice. Overall, these findings suggest that TPNP could be used to develop natural multifunctional nanoplatforms for molecular therapy of AS and other inflammation-related diseases.

A Robust and Efficient Method to Purify DNA-Scaffolded Nanostructures by Gravity-Driven Size Exclusion Chromatography.

In recent decades, nucleic acid self-assemblies have emerged as popular nanomaterials due to their programmable and robust assembly, prescribed geometry, and versatile functionality. However, it remains a challenge to purify large quantities of DNA nanostructures or DNA-templated nanocomplexes for various applications. Commonly used purification methods are either limited by a small scale or incompatible with functionalized structures. To address this unmet need, we present a robust and scalable method of purifying DNA nanostructures by Sepharose resin-based size exclusion. The resin column can be manually packed in-house with reusability. The separation is driven by a low-pressure gravity flow in which large DNA nanostructures are eluted first followed by smaller impurities of ssDNA and proteins. We demonstrated the efficiency of the method for purifying DNA origami assemblies and protein-immobilized DNA nanostructures. Compared to routine agarose gel electrophoresis that yields 1 µg or less of purified products, this method can purify ∼100-1000 µg of DNA nanostructures in less than 30 min, with the overall collection yield of 50-70% of crude preparation mixture. The purified nanocomplexes showed more precise activity in evaluating enzyme functions and antibody-triggered activation of complement protein reactions.

Photoionization cross sections measurements of the excited states of lutetium and ytterbium in the near threshold region.

In this work, the threshold photoionization cross sections from the excited states of lutetium and ytterbium atoms were investigated by the laser pump-probe scheme under the condition of saturated resonant excitation. We obtained the resonance enhanced multiphoton ionization spectra of the lutetium and ytterbium atoms of the lanthanide metals in the range of 307.50-312.50 nm and 265.00-269.00 nm, respectively; the photoionization cross sections of the 5d6s(1D)6p(2D05/2) and 5d6s(3D)6p(2P01/2) states of lutetium and the 4f13(2F0)5d6s2(J = 1) states of ytterbium above threshold regions (0.4-1.6 eV) were measured, and measured values ranged from 2.3 ± 0.2 to 17.7 ± 1.5 Mb.

Adverse effects of microparticles on transfusion of stored red blood cell concentrates.

BACKGROUND: Systemic and pulmonary coagulopathy and inflammation are important characteristics of transfusion-related acute lung injury (TRALI). Whether microparticles that accumulate in transfused red blood cell concentrates (RBCs) have proinflammatory and procoagulant potential and contribute to adverse reactions of RBC transfusions is unclear. AIM: To investigate the ability of microparticles in stored RBCs to promote thrombin generation and induce human pulmonary microvascular endothelial cell (HMVEC) activation and damage. METHODS: The number and size of microparticles were determined by flow cytometric and nanoparticle tracking analyses, respectively. Thrombin generation and the intrinsic coagulation pathway were assayed by a calibrated automated thrombogram and by measuring activated partial thromboplastin time (aPTT), respectively. The expression of ICAM-1 and the release of cytokines by endothelial cells were detected by flow cytometric analyses. HMVEC damage was assessed by incubating lipopolysaccharide-activated endothelial cells with MP-primed polymorphonuclear neutrophils (PMNs). RESULTS: The size of the microparticles in the RBC supernatant was approximately 100-300 nm. Microparticles promoted thrombin generation in a dose-dependent manner and the aPTT was shortened. Depleting microparticles from the supernatant of RBCs stored for 35 days by either filtration or centrifugation significantly decreased the promotion of thrombin generation. The expression of ICAM-1 on HMVECs was increased significantly by incubation with isolated microparticles. Furthermore, microparticles induced the release of interleukin-6 (IL-6) and interleukin-8 (IL-8) from HMVECs. Microparticles induced lipopolysaccharide-activated HMVEC damage by priming PMNs, but this effect was prevented by inhibiting the PMNs respiratory burst with apocynin. CONCLUSION: Microparticles in stored RBCs promote thrombin generation, HMVEC activation and damage which may be involved in TRALI development.

Nano-Drug Delivery Systems Targeting CAFs: A Promising Treatment for Pancreatic Cancer.

Currently, pancreatic cancer (PC) is one of the most lethal malignant tumors. PC is typically diagnosed at a late stage, exhibits a poor response to conventional treatment, and has a bleak prognosis. Unfortunately, PC's survival rate has not significantly improved since the 1960s. Cancer-associated fibroblasts (CAFs) are a key component of the pancreatic tumor microenvironment (TME). They play a vital role in maintaining the extracellular matrix and facilitating the intricate communication between cancer cells and infiltrated immune cells. Exploring therapeutic approaches targeting CAFs may reverse the current landscape of PC therapy. In recent years, nano-drug delivery systems have evolved rapidly and have been able to accurately target and precisely release drugs with little or no toxicity to the whole body. In this review, we will comprehensively discuss the origin, heterogeneity, potential targets, and recent advances in the nano-drug delivery system of CAFs in PC. We will also propose a novel integrated treatment regimen that utilizes a nano-drug delivery system to target CAFs in PC, combined with radiotherapy and immunotherapy. Additionally, we will address the challenges that this regimen currently faces.

Controlling spatial distribution of functional lipids in a supported lipid bilayer prepared from vesicles.

Conjugating biomolecules, such as antibodies, to bioconjugate moieties on lipid surfaces is a powerful tool for engineering the surface of diverse biomaterials, including cells and nanoparticles. We developed supported lipid bilayers (SLBs) presenting well-defined spatial distributions of functional moieties as models for precisely engineered functional biomolecular-lipid surfaces. We used quartz crystal microbalance with dissipation (QCM-D) and atomic force microscopy (AFM) to determine how vesicles containing a mixture of 1,2-dipalmitoyl-sn-glycero-3-phosphatidylcholine (DPPC) and 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-N-[azido(polyethylene glycol)-2000] (DSPE-PEG-N3) form SLBs as a function of the lipid phase transition temperature (Tm). Above the DPPC Tm, DPPC/DSPE-PEG-N3 vesicles form SLBs with functional azide moieties on SiO2 substrates via vesicle fusion. Below this Tm, DPPC/DSPE-PEG-N3 vesicles attach to SiO2 intact. Intact DPPC/DSPE-PEG-N3 vesicles on the SiO2 surfaces fuse and rupture to form SLBs when temperature is brought above the DPPC Tm. AFM studies show uniform and complete DPPC/DSPE-PEG-N3 SLB coverage of SiO2 surfaces for different DSPE-PEG-N3 concentrations. As the DSPE-PEG-N3 concentration increases from 0.01 to 6 mol%, the intermolecular spacing of DSPE-PEG-N3 in the SLBs decreases from 4.6 to 1.0 nm. The PEG moiety undergoes a mushroom to brush transition as DSPE-PEG-N3 concentration varies from 0.1 to 2.0 mol%. Via copper-free click reaction, IgG was conjugated to SLB surfaces with 4.6 nm or 1.3 nm inter-DSPE-PEG-N3 spacing. QCM-D and AFM data show; 1) uniform and complete IgG layers of similar mass and thickness on the two types of SLB; 2) a higher-viscosity/less rigid IgG layer on the SLB with 4.6 nm inter-DSPE-PEG-N3 spacing. Our studies provide a blueprint for SLBs modeling spatial control of functional macromolecules on lipid surfaces, including surfaces of lipid nanoparticles and cells.

Physicochemical Targeting of Lipid Nanoparticles to the Lungs Induces Clotting: Mechanisms and Solutions.

Lipid nanoparticles (LNPs) have become the dominant drug delivery technology in industry, holding the promise to deliver RNA to up or down-regulate any protein of interest. LNPs have mostly been targeted to specific cell types or organs by physicochemical targeting in which LNP's lipid compositions are adjusted to find mixtures with the desired tropism. Here lung-tropic LNPs are examined, whose organ tropism derives from containing either a cationic or ionizable lipid conferring a positive zeta potential. Surprisingly, these LNPs are found to induce massive thrombosis. Such thrombosis is shown in the lungs and other organs, and it is shown that it is greatly exacerbated by pre-existing inflammation. This clotting is induced by a variety of formulations with cationic lipids, including LNPs and non-LNP nanoparticles, and even by lung-tropic ionizable lipids that do not have a permanent cationic charge. The mechanism depends on the LNPs binding to and then changing the conformation of fibrinogen, which then activates platelets and thrombin. Based on these mechanisms, multiple solutions are engineered that enable positively charged LNPs to target the lungs while ameliorating thrombosis. The findings illustrate how physicochemical targeting approaches must be investigated early for risks and re-engineered with a careful understanding of biological mechanisms.

Excellent Polymerized Ionic-Liquid-Based Gel Polymer Electrolytes Enabled by Molecular Structure Design and Anion-Derived Interfacial Layer.

Polymerized ionic liquid (PIL)-based gel polymer electrolytes (GPEs) are well known as highly safe and stable electrolytes but with low ambient ionic conductivity. Herein, we first designed and synthesized an IL monomer with a long and flexible side chain and then mixed it with LiTFSI and MEMPTFSI to construct a PIL-based GPE (denoted as GM-GPE). The special molecular structure of the monomer greatly improves the ionic transport through the PIL chain, and the introduction of MEMPTFSI plasticizer further improves the ionic conductivity, promoting a TFSI--anion-derived SEI formation to suppress Li dendrite growth and forming an electrostatic shielding effect of MEMP+ cations to promote the uniform deposition of Li+. Consequently, the as-prepared GM-GPE exhibits high ambient ionic conductivity (4.3 × 10-4 S cm-1, 30 °C), robust electrochemical stability, excellent thermal stability, nonflammability, and superior ability to inhibit Li dendrite growth. The resultant LiFePO4|GM-GPE|Li cell exhibits a high discharge capacity of 150 mA h g-1 at 0.2 C along with a good cycling stability and rate capability. This work brings about new guidance for the development of high-quality GPEs with high ionic conductivity, high stability, and safety for long cycling and dendrite-free lithium metal batteries.

Nrf2-mediated redox balance alleviates LPS-induced vascular endothelial cell inflammation by inhibiting endothelial cell ferroptosis.

Ferroptosis plays an important role in inflammation and oxidative stress. Whether ferroptosis is involved in the inflammation of vascular endothelial cells and its regulation mechanism remains unclear. We estimated the correlation between serum iron ion levels and the inflammation index of 33 patients with arteriosclerosis. In vitro, HUVECs with or without ferrostatin-1 were exposed to Lipopolysaccharide. Corresponding cell models to verify the target signaling pathway. The results showed that serum iron ion levels had a significant positive correlation with N ratio, N/L, LDL level, and LDL/HDL (P < 0.05), and a negative correlation with L ratio (P < 0.05) in the arteriosclerosis patients. In vitro, ferroptosis is involved in HUVECs inflammation. Ferrostatin-1 can rescue LPS-induced HUVECs inflammation by decreasing HMGB1/IL-6/TNF-α expression. Nrf2 high expression could protect HUVECs against ferroptosis by activating the GPX4/GSH system, inhibiting ferritinophagy, and alleviating inflammation in HUVECs by inhibiting HMGB1/IL-6/TNF-α expression. It also found that Nrf2 is a key adaptive regulatory factor in the oxidative damage of HUVECs induced by NOX4 activation. These findings indicated that ferroptosis contributed to the pathogenesis of vascular endothelial cell damage by mediating endothelial cell inflammation. Nrf2-mediated redox balance in vascular inflammation may be a therapeutic strategy in vascular diseases.