The C-reactive protein-triglyceride-glucose index (CTI) is a novel biomarker that integrates measures of insulin resistance and inflammation. Its association with cardiovascular disease (CVD) risk across various glycemic statuses remains unclear. This prospective study included 7,584 middle-aged and elderly participants from the China Health and Retirement Longitudinal Study (CHARLS). CTI was calculated using the formula 0.412*Ln(CRP) + Ln(TG × FPG)/2. Cox proportional hazards models and restricted cubic splines were employed to evaluate the relationship between CTI and CVD risk, with subgroup analyses conducted based on gender, age, and glycemic status. Over a median follow-up period of 108.1 months, 1,989 participants (26.23

Molecular imaging based on paramagnetic nanoagents has emerged as an intriguing strategy to sensitize the local magnetic properties of pivotal pathological processes related to atherosclerotic plaque destabilization, opening up a potential possibility for noninvasively predicting plaque vulnerability. Unfortunately, current magnetic resonance (MR) imaging interpretation fails to provide objectively and precisely quantitative imaging descriptors, thus showing limited values in stratifying the plaque risk from MR images. To address this need, we originated a synergistic nanoagents (tFM-Nanoagents)-assisted machine learning (nano-AML) technology for directly reading out plaque vulnerability from molecular high-resolution vessel wall MR imaging (HR-VWI). The proposed diagnostic paradigm provided a holistic visualization of the distribution of foamy macrophage-defined plaques; by using a machine learning (ML) approach to decode data of tFM-Nanoagents sensitized HR-VWI, an imaging-derived risk score (nano-AML score) correlating with the pathology vulnerability index of plaques was generated and validated in a preclinical atherosclerotic model. Our data showed that the nano-AML score could effectively phenotype plaques into "vulnerable" and "stable" classes, with an area under the curve (AUC) of 0.871 in the training cohort and 0.870 in the validation cohort. We also demonstrated that the predictive performance of nano-AML score outperformed that of commercial contrast agent Gadovist (AUC of 0.560 in the training cohort and 0.538 in the validation cohort), suggesting its robust potency for serving as a reliable predictor for vulnerable plaques.

While restoring blood flow is the primary treatment for acute myocardial infarction (AMI), this process often triggers additional damage known as myocardial ischemia/reperfusion injury (MIRI). Recent studies have suggested that regulated cell death is a major contributor to cardiomyocyte injury during ischemia and subsequent reperfusion. Notably, emerging evidence has demonstrated that both ferroptosis and pyroptosis play important roles in the pathogenesis of MIRI. Ferroptosis is primarily driven by iron-dependent lipid peroxidation, whereas pyroptosis is characterized by inflammasome-mediated inflammatory cell death. However, these processes are typically studied independently, and their potential interactions and shared regulatory mechanisms remain unclear. In this review, we comprehensively summarize the molecular mechanisms underlying ferroptosis and pyroptosis in MIRI. We also discuss emerging evidence supporting the crosstalk between these two processes, with a particular focus on shared upstream triggers such as reactive oxygen species (ROS), mitochondrial dysfunction, and common regulatory proteins, including nuclear factor erythroid 2-related factor 2 (Nrf2), p53, and members of the high mobility group box (HMGB) family. Furthermore, we highlight current therapeutic strategies targeting ferroptosis and pyroptosis and explore the potential of dual-targeting approaches based on their shared signaling pathways. A deeper understanding of the interplay between these two forms of cell death may provide novel insights into the pathogenesis of MIRI and support the development of more effective cardioprotective strategies.

Ferritinophagy is a selective form of macroautophagy/autophagy that mediates the degradation of ferritin complexes, releasing stored iron, and maintaining intracellular iron homeostasis. Proper regulation of ferritinophagy is essential for cellular adaptation to metabolic stress, whereas dysregulation disrupts iron balance and contributes to pathological processes. Excessive ferritinophagy leads to iron overload and reactive oxygen species accumulation, driving oxidative stress, ferroptosis, and inflammation, which are key contributors to cellular injury and progressive organ dysfunction. Despite advances in our understanding of autophagy and ferroptosis, the specific role of ferritinophagy in organ-specific injury remains unclear. In this review, we provide a comprehensive overview of the molecular mechanisms of ferritinophagy and critically examine its emerging roles in the pathogenesis of injuries to the heart, liver, lungs, and kidneys. We further highlight the therapeutic potential of targeting ferritinophagy and propose future research directions aimed at harnessing this pathway for the treatment of organ injuries.Abbreviations: 3-MA: 3-methyladenine; ACO1/IRP1: aconitase 1; AKI: acute kidney injury; ARDS: acute respiratory distress syndrome; ATG: autophagy related; BECN1: beclin 1; CARM1/PRMT4: coactivator associated arginine methyltransferase 1; CIRBP: cold inducible RNA binding protein; CKD: chronic kidney disease; COPD: chronic obstructive pulmonary disease; ELAVL1: ELAV like RNA binding protein 1; Fer-1: ferrostatin-1; FTH1: ferritin heavy chain 1; GABARAP: GABA type A receptor-associated protein; GPX4: glutathione peroxidase 4; HAMP/hepcidin: hepcidin antimicrobial peptide; HCC: hepatocellular carcinoma; HERC2: HECT and RLD domain containing E3 ubiquitin protein ligase 2; HSCs: hepatic stellate cells; IL13: interleukin 13; IL6: interleukin 6; I/R: ischemia-reperfusion; IRE: iron-responsive element; IREB2/IRP2: iron responsive element binding protein 2; LPS: lipopolysaccharide; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MDA: malondialdehyde; MIOX: myo-inositol oxygenase; NCOA4: nuclear receptor coactivator 4; NFE2L2/Nrf2: NFE2 like bZIP transcription factor 2; ROS: reactive oxygen species; SIRT1: sirtuin 1; SLC40A1/ferroportin: solute carrier family 40 member 1; STAT3: signal transducer and activator of transcription 3; STEAP3: STEAP3 metalloreductase; TFRC/TfR1: transferrin receptor; USP11: ubiquitin specific peptidase 11; YAP1: Yes1 associated transcriptional regulator.

ABSTRACT Hypertension exhibits variability in diagnosis and treatment across phenotypes. Obesity and metabolic disorders are key risk factors, interacting with inflammatory states. This study explores their associations with hypertension phenotypes and the mediating role of inflammation. This study analyzed 17 158 participants from NHANES (2007–2018). Hypertension phenotypes were diagnosed per guidelines. Associations were evaluated using weighted generalized linear models, with the receiver operating characteristic(ROC) curves identifying optimal obesity indices. Stratified analyses were conducted by gender, lifestyle, and diet. Mediation analysis assessed inflammation's role. Among six obesity indicators, Weight‐Waist Index (WWI) was better for Isolated Systolic Hypertension (ISH) (area under curve[AUC]:0.64, 95%confidence interval[CI]:0.62–0.67), Waist Circumference (WC) was better for Isolated Diastolic Hypertension (IDH) (AUC:0.68, 95%CI:0.67–0.69). High obesity indicators (WC for IDH, WWI for ISH and WC for SDH) without metabolic disorders linked to IDH (odds ratio[OR] 3.02, 95% CI 1.57–5.82), not ISH or Systolic‐Diastolic Hypertension (SDH) (p > 0.05). High obesity indicators (WC for IDH, WWI for ISH and WC for SDH) with metabolic disorders associated with all phenotypes (IDH: OR 3.62, 95% CI 2.19–5.97; ISH: OR 1.76, 95% CI 1.09–2.84; SDH: OR 2.04, 95% CI 1.25–3.34). Inflammation mediated partially: 6.44% via RBC in IDH (non‐obesity metabolic disorders, P < 0.001), 18.4% via Monocyte in ISH (obesity without metabolic disorders, P < 0.05). Stratified analyses showed phenotype‐specific differences: IDH nonsignificant, ISH by smoking, SDH by age. High WC without metabolic disorders is linked to IDH, while metabolically disordered obesity correlates with all phenotypes. These effects are mediated by distinct variables, aiding phenotype‐specific diagnosis and treatment.

The conceptual landscape of cell death has evolved beyond the traditional dichotomy of apoptosis and necrosis to encompass diverse regulated pathways including necroptosis, autophagy, ferroptosis, and pyroptosis. Necroptosis, a caspase-independent inflammatory form of programmed cell death, has emerged as a critical driver of the pathogenesis of cardiovascular disorders, neurodegenerative diseases, and cancer. Concurrently, our understanding of mitochondrial biology has undergone a paradigm shift: mitochondria are no longer viewed merely as bioenergetic powerhouses, but as dynamic signalling hubs that orchestrate metabolic reprogramming, cellular homeostasis, and ultimate cell fate decisions. In this regard, a growing body of evidence suggests that mitochondrial dysfunction is a central rheostat that enables necroptotic execution. This review delineates the mechanistic interplay between necroptosis and mitochondrial dysfunction and systematically analyzes the key molecular mediators and pathological pathways through which mitochondrial dysregulation drives necroptotic activation. Furthermore, this review identifies actionable therapeutic targets and translational strategies for modulating necroptosis in related diseases.

Background As a key glycolytic enzyme, Pyruvate kinase M2 (PKM2), which is highly expressed in cancer cells, promotes hepatocellular carcinoma (HCC) proliferation/metastasis. This research investigates the involvement of Ubiquitin protein ligase E3 component N-recognin 7 (UBR7) in HCC progression/glycolysis and its potential mechanisms. Methods UBR7 expressions in HHL-5, Huh-7, and HepG2 cells were investigated using Quantitative Reverse Transcription Polymerase Chain Reaction and Western Blot. Cell counting kit-8, clone formation experiment, scratch-wound assay, and transwell testing were conducted to assess the malignant biological behaviors of HepG2 and Huh-7 cells; the absorption level of glucose and generation levels of lactic acid and ATP were tested by assay kits. Huh-7 cells with stably overexpressed or knocked down UBR7 were inoculated into nude mice. Regular measurements were conducted on the tumor size, the tumors were isolated and weighed on the 35th day, and the glycolytic level in the tumor tissues was determined. Results In HCC cells, UBR7 was significantly downregulated. Notably, UBR7 knockdown promoted HCC progression and glycolysis, increasing the viability of HepG2 and Huh-7 cells by 23%u201324% (p u0026lt; 0.001), whereas UBR7 overexpression exerted the opposite inhibitory effects, resulting in a reduction of about 19%u201331% in cell viability (p u0026lt; 0.001). UBR7 knockdown upregulated PKM2 expression in HCC cells, while UBR7 overexpression led to a marked reduction in PKM2 levels. Importantly, PKM2 overexpression partly abrogated the inhibitory impacts of UBR7 on HCC progression and glycolysis. In vivo experiments further demonstrated that UBR7 overexpression suppressed tumor growth and hindered glycolysis in nude mice. Conclusion UBR7 suppressed PKM2 expression, thus hindering malignant biological progression and glycolysis in HCC, providing a potential therapeutic target for HCC treatment.

Usher syndrome type 1B (USH1B) is a rare autosomal recessive disorder characterized by congenital deafness, vestibular dysfunction, and progressive retinitis pigmentosa (RP). Cystoid macular edema (CME) is a treatable complication of RP, but its management in young children with USH1B lacks evidence-based guidance. We report the first observation of spontaneous CME resolution in a pediatric USH1B patient managed conservatively with refractive correction and close follow-up, accompanied by accelerated axial elongation exceeding age-matched normative rates. A 3-year-old male with a genetic diagnosis of USH1B (compound heterozygous MYO7A mutations: c.640G > A p.Gly214Arg and c.6026 C > T p.Ala2009Val) presented with bilateral CME detected on optical coherence tomography (OCT). Baseline examination revealed high myopia (spherical equivalent refraction: -6.50D right, -5.75D left) and axial lengths of 24.19 mm and 24.06 mm, respectively. Given the lack of pediatric treatment guidelines, a conservative approach with full-time refractive correction and close monitoring was adopted. After 9 months of follow-up, OCT demonstrated spontaneous and near-complete resolution of bilateral CME without any pharmacological or surgical intervention. Best-corrected visual acuity remained stable at 0.3–0.4. Notably, axial length increased to 24.31 mm and 24.21 mm, corresponding to a growth rate of 0.027 mm/month, which exceeds the age-matched normative range (0.016–0.025 mm/month). This case provides the first documentation of spontaneous CME resolution in a pediatric USH1B patient managed conservatively. It suggests that a period of observation with refractive correction may be a prudent initial strategy, avoiding unnecessary exposure to potential treatment-related risks. The concurrent observation of accelerated axial elongation highlights the importance of including myopia progression monitoring in the ophthalmic follow-up of pediatric USH patients.

Organic crystalline scintillators have attracted significant attention for their low processing temperatures, cost-effectiveness, and tunable optical properties, making them strong candidates for advanced medical imaging. However, organic crystalline scintillators, constrained by their poor crystallinity, can only be employed after being ground into powder for forming scintillator screens, rather than being used directly as bulk crystals for scintillation imaging, which severely compromises their intrinsic optical performance and imaging resolution. In this study, pure and four doped anthracene crystals with dimensions of phi 15 & times; 60 mm were successfully grown using an improved Bridgman thermal field technique. In particular, the crystalline quality of the resulting benz[a]anthracene-doped and chrysene-doped anthracene crystals was superior to that of the pure anthracene crystal. Transparent organic crystal wafer scintillator screens were subsequently fabricated by cutting and polishing technologies. Performance characterization demonstrated that benz[a]anthracene-doped and chrysene-doped anthracene crystals exhibited radioluminescence intensity threefold and fivefold that of the host, respectively. The chrysene-doped anthracene crystal achieved a light yield of 50 976 photons MeV- 1, a detection limit of 0.11 & micro;Gy s- 1, and an ultra-high spatial resolution of 20 lp mm- 1. This work demonstrates molecular doping's ability to modulate properties, opening a new avenue for high-resolution scintillator screens.

The coupled impairment of the cerebrovascular network and the glymphatic system is a critical pathological feature of stroke. However, comprehensively assessing this dual-pathway damage remains a significant clinical challenge. Current clinical MRI contrast agents are fundamentally limited by single-modality contrast, restricted sequence compatibility, and safety concerns, falling short of multi-parametric evaluation at clinical 3.0 T magnetic fields. To address this gap, we propose an integrated multi-sequence MRI strategy enabled by a highly translatable, bovine serum albumin (BSA)-templated Fe3O4 nanoprobe (MS-Fe3O4-Nanoagents). Rather than employing complex nanoarchitectures, we utilized a minimalist biomimetic co-precipitation approach to yield ultrasmall Fe3O4 cores (∼4.5 nm) with an optimized hydrated diameter (∼20 nm). The BSA shell creates a hydrophilic, exchange-rich interface that modulates the rotational motion of water protons, achieving a balanced T1-T2 dual-modal contrast profile (r1 = 11, r2 = 59, and r2* = 131 mM-1 s-1 at 3.0 T) with an optimal r2/r1 ratio. Phantom and in vivo MRI confirmed that the administration of MS-Fe3O4-Nanoagents robustly drives multi-sequence signal modulation-enhancing T1-weighted/mapping signals while effectively attenuating T2/SWI signals. In rat models of ischemic and hemorrhagic stroke, the versatile compatibility of this nanoprobe significantly amplified the signal-to-noise ratio and spatial resolution across multiple sequences. This capability enabled the dynamic and quantitative mapping of venous hemodynamics, microbleeds, blood-brain barrier (BBB) disruption, and delayed glymphatic clearance without the need for sequence-specific contrast agents. By repurposing a biocompatible nanomaterial into a unified multi-sequence platform, this study provides a robust diagnostic tool for the precise prognostic evaluation and therapeutic monitoring of complex post-stroke injuries.

Lung fibrosis progression is marked by impaired alveolar epithelial regeneration and uncontrolled myofibroblast differentiation, though the underlying mechanisms remain poorly understood. In this study, we discovered that Atg5 was upregulated in the mesenchymal cells of lungs from both patients with idiopathic pulmonary fibrosis (IPF) and mice with bleomycin (BLM)-induced fibrosis. Selective deletion of Atg5 in lung mesenchymal cells increased the susceptibility of mice to BLM-induced lung fibrosis. Mechanistically, the loss of Atg5 promoted transforming growth factor β 1 (TGF-β1)-induced oxidative stress and cellular senescence in fibroblasts, myofibroblast differentiation, and extracellular matrix deposition. Intriguingly, loss of Atg5 impaired the secretion of tissue repair-favoring factors in fibroblasts, causing defects in the proliferation and differentiation of alveolar type 2 cells. This study showed that Atg5 is essential for alveolar epithelial repair and myofibroblast control in lung fibrosis.

Currently, cuproptosis has garnered significant interest in tumor postoperative therapy. However, cuproptosis is profoundly influenced by the homeostasis of the tumor microenvironment (TME), significantly diminishing therapeutic efficacy. Herein, we engineered a botanical/nanozyme-engineered hydrogel (baicalein/Cu-TCPP/CuO2 hydrogel, BTCH) to achieve boosting cuproptosis via dual tumor homeostasis remodeling for postoperative breast cancer management. In vitro studies demonstrated that the BTCH hydrogel could initiate efficient Fenton-like reactions via POD-like activity to generate cytotoxic •OH in weakly acidic TME and consume endogenous GSH via GSHOx-like mimetic activity, thereby disrupting redox homeostasis. Notably, baicalein could elicit an anti-Warburg effect for interfering with the energy metabolic homeostasis. The dual energy metabolism/redox homeostasis modulation resulted in a significant elevation in cuproptosis. In vivo studies demonstrated that the BTCH hydrogel could not only potentiate the cuproptosis-triggered residual tumor deletion but also effectively combat surgical site infections and accelerate postoperative wound regeneration, thereby achieving suppression of tumor recurrence and metastasis. Furthermore, multi-omics analyses revealed that this combination therapy precipitated significant alterations in tumor energy metabolism and disrupted redox homeostasis for boosting cuproptosis. By integrating multiple anti-tumor, antibacterial, and wound-healing functionalities into a single platform, this hydrogel overcame the limitations of conventional monomodal therapies, demonstrating great application potential for postoperative breast cancer management.

Nanohydroxyapatite (nHA) is a highly promising candidate for sustainable agriculture due to its excellent biocompatibility and environmental friendliness. However, their practical application has long been hindered by poor dispersibility. Herein, we develop an in situ approach that couples phosphorylated carbon sphere (PCS) formation from waste orange peels with concurrent nHA nucleation, creating nHA/PCS composites as a root exudate-triggered nanofertilizer. Density functional theory (DFT) calculations show weak binding energy at the nHA/PCS-nHA interface, thereby inhibiting nHA nanorods agglomeration. Compared to commercial nanohydroxyapatite (nCHA), nHA/PCS demonstrates superior interface stability and sustained-release properties. The nHA/PCS treatment significantly enhances lettuce seedling growth by improving root architecture and stimulating oxalic acid secretion, increasing leaf fresh weight by 60.95% compared to that with nCHA treatments. As a scaffold, the PCS matrix chemically anchors nHA nanorods for a controlled release in response to root exudates. This work presents an innovative strategy for engineering stable nanofertilizer delivery systems.

Background & Objective: The prognosis of lung adenocarcinoma (LUAD) remains poor, primarily due to treatment resistance and a lack of effective biomarkers. This research investigated the potential of ubiquitination-related genes (UbRG) as prognostic indicators for LUAD. Methodology: This study was conducted at Tianjin Medical University Cancer Institute and Hospital from May 2025 to October 2025. Leveraging data from TCGA, we initially employed WGCNA to identify key modules of UbRG associated with LUAD. Then, a multigene prognostic signature was developed. To investigate the mechanisms, GSEA and CIBERSORT were used to detect activated signaling pathways and immune landscape, respectively. Finally, drug sensitivity analysis was performed. Results: Our analysis identified nine gene pairs that constitute the UbRG prognostic signature, with individuals in the high-risk cohort generally experiencing worse outcomes. Pathway enrichment analyses revealed immune response pathways in the low-risk cohort and the cell cycle and DNA replication pathways in the high-risk cohort. CIBERSORT revealed distinct immune cell distributions, with more CD4(+) T cells and DCs in the low-risk cohort. Drug sensitivity analysis suggest that the low-risk group may exhibit a greater sensitivity to both chemotherapy and targeted treatments. Conclusion: This study presents a novel UbRG signature for LUAD prognosis, emphasizing the role of ubiquitination in the immune response. These findings may guide future therapeutic strategies in LUAD.

The triglyceride-glucose (TyG) index has been recognized as a surrogate marker for insulin resistance (IR) and an independent risk factor for cardiovascular disease (CVD). However, the combined effect of the TyG index and visceral obesity on CVD incidence remains unclear. We aimed to investigate the interaction, joint association, and potential mediators between the TyG index and comprehensive anthropometric indices with CVD risk in middle-aged and older adults. We analyzed 7046 participants aged ≥ 45 years without baseline CVD from the China Health and Retirement Longitudinal Study (CHARLS) over a 9-year follow-up period. Retrospective collection included sociodemographic details, health status, physical examination results, and blood biomarkers. Adjusted Cox proportional hazards models were used to examine the interaction between TyG levels and anthropometric indices and their joint associations with CVD incidence. Subgroup analyses were conducted to evaluate the associations across different populations, and mediation analysis was performed to identify potential mediating pathways. The predictive value was determined using the area under the curve (AUC) of receiver operating characteristic curves. In addition, we validated the findings in the Multi-Ethnic Study of Atherosclerosis (MESA) cohort. In the CHARLS study, 1768 (25.1

OBJECTIVE:To establish a homogeneous immunoassay for quantitative detection of total procollagen type 1 n-terminal propeptide (P1NP) in human serum. METHODS:The assay was established after screening raw materials and optimizing the reaction conditions, and the performance of the assay was evaluated according to the clinical guidelines. Meanwhile, the detection results of the established assay were compared with those of the Roche electrochemiluminescence immunoassay. RESULTS:The coefficient of variation was 4.20 % ∼9.37 %, and the intermediate precision was 6.20 % ∼9.80 %. The limit of blank (LoB) was 1.14 ng/mL, and the limit of quantification (LoQ) was 3.83 ng/mL. The linear range was 5.88 ng/mL ∼1447.65 ng/mL. The correlation coefficient (r) between the results of the established total P1NP-LiCA and the Roche ECLIA was 0.8969. CONCLUSIONS:A homogeneous quantitative immunoassay for total P1NP was developed, which could be used as a practical and cost-effective alternative for routine clinical use in assessing bone formation markers.

BackgroundType 2 diabetes mellitus (T2DM) is a major risk factor for pulmonary tuberculosis (PTB), exacerbates disease severity and reduces the efficacy of anti-tuberculosis therapy. Previous studies have shown that T2DM is associated with exacerbated metabolic disturbances in patients with PTB. However, metabolic differences between PTB patients with comorbid T2DM (PTB-DM) and those with PTB after anti-TB therapy remain unclear.MethodsUntargeted metabolomic analysis was conducted on plasma samples collected from April 2024 to November 2025 at Tianjin Haihe Hospital, China. A total of 75 participants were enrolled, including healthy controls, patients with newly diagnosed drug-sensitive PTB, patients with PTB-DM, as well as two independent post-treatment groups sampled after 6 months of standard anti-TB therapy: patients with PTB and patients with PTB-DM.ResultsPatients with PTB exhibited marked metabolic disturbances, particularly in tyrosine metabolism and steroid hormone biosynthesis. Patients with PTB-DM showed broader metabolic reprogramming, including changes in arginine and proline metabolism, steroid hormone biosynthesis, cAMP signaling, and taurine and hypotaurine metabolism. After 6 months of standard therapy, the PTB_6M group showed treatment-associated metabolic differences, especially in bile acid metabolism, suggesting partial normalization of several metabolic features. In contrast, patients with PTB-DM after treatment showed persistent metabolic abnormalities involving sphingolipid, purine and biotin metabolism. Notably, 12-HETE and 12-HHTrE showed elevated levels in active PTB, decreased levels after treatment, but remained relatively higher in PTB-DM after treatment.ConclusionsThis study offers an integrated assessment of metabolic alterations in PTB and PTB-DM, suggesting that comorbid T2DM is associated with broader metabolic dysregulation during active PTB and persistent post-treatment metabolic abnormalities.

The postoperative therapy for breast cancer is significantly restricted by local immunosuppression and the non-healing of infected wounds. We developed a botanical/nanozyme/polysaccharide metabolic immunomodulator (BCZG), using alginate as the primary scaffold, integrating baicalein-loaded carbon nanozyme into a polydopamine-modified alginate hydrogel. In the acidic tumor microenvironment, the BCZG mimicked NOX, OXD, and GSHOx activities, which could deplete NADH/ATP and glutathione to block heat shock protein synthesis and amplify ROS storms for achieving robust immunogenic cell death. Meanwhile, the loaded baicalein as a heat shock protein inhibitor synergistically enhanced PTT sensitivity in conjunction with the energy metabolism-blocking effect of the nanozymes. In the neutral/alkaline wound microenvironment, the BCZG hydrogel switched to catalase- and superoxide dismutase-like activities, scavenging excess ROS, relieving inflammation, and exerting potent antibacterial effects to promote postoperative wound healing. The alginate-based biomimetic nanozyme system disrupted the vicious cycle of wound infection, persistent inflammation, immunosuppressive niche formation, and tumor recurrence. Consequently, it reprogrammed energy metabolism and activated antitumor immunity, offering a novel strategy for postoperative breast cancer treatment.