In this study, integrated proteomic and transcriptomic analyses identified peroxiredoxin 1 (PRDX1) as a novel urinary biomarker for bladder cancer (BC). PRDX1 was significantly upregulated in BC tissues and was associated with poorer overall survival. In vitro experiments further demonstrated that PRDX1 promotes malignant phenotypes of BC cells, including proliferation, migration, and invasion. Silencing PRDX1 in BC cells significantly reduced the invasiveness and proliferation ability.To address the clinical need for rapid and non-invasive detection, we developed an innovative optical fiber biosensor based on surface plasmon resonance (SPR) technology for the quantitative detection of urinary PRDX1. The biosensor exhibited excellent analytical performance, including high sensitivity (limit of detection: 0.06 ng/mL), a wide linear range (0-25 ng/mL), rapid response (∼14 s), as well as good stability and selectivity. In clinical validation involving 97 BC patients and 30 healthy controls, the biosensor demonstrated outstanding diagnostic performance, with an area under the receiver operating characteristic curve (AUC) of 0.91 and an overall diagnostic accuracy of 86.6%, outperforming conventional enzyme-linked immunosorbent assay (ELISA). Collectively, this study not only identifies PRDX1 as a promising biomarker for non-invasive diagnosis and prognostic evaluation of BC, but also establishes an efficient SPR-based optical fiber sensing platform, providing new insights into both clinical detection and the functional role of PRDX1 in BC progression.

Robot-assisted urologic surgery attenuates the tactile and kinesthetic information normally generated by tissue contact, but the organization and scope of the related literature remain unclear. We mapped publication activity, collaboration, citation structure, and thematic change in research involving haptic feedback and force information. Web of Science Core Collection was searched on 24 July 2026 using a proximity-based robotic-urology block combined with terms for tactile or kinesthetic feedback, force sensing or estimation, force control, and sensory substitution. Seventy-four English-language articles and reviews published in 2001–2025 were analyzed with bibliometrix/Biblioshiny and CiteSpace. The corpus comprised 50 journals, 442 authors, 222 author keywords, and 2,335 cited references; 13 papers were published in 2025. The United States led output and network brokerage, and author participation was dispersed, with 89.59

Acute kidney injury (AKI) lacks disease-modifying therapies, partly because cell type–specific injury programs remain incompletely resolved and tissue mechanisms are not readily translated into clinically accessible biomarkers. We constructed a cross-scale, multi-omics atlas to prioritize candidate regulator linking renal injury circuitry with urine-detectable signals. Human single-cell, bulk, and spatial transcriptomics were integrated with mouse renal ischemia–reperfusion injury (RIRI) kidney proteomics and clinical urine proteomics. Overlap of differentially expressed genes and differentially abundant proteins nominated candidates, which were ranked by a random forest model. Immune remodeling was assessed by deconvolution and pathway enrichment, with spatial localization supported by reference-based deconvolution. Therapeutic tractability was explored by structure-based virtual screening, molecular docking, molecular dynamics simulation, and cellular thermal shift assay (CETSA). TRIM28 was evaluated in HK-2 hypoxia/reoxygenation (H/R) and mouse RIRI models using genetic perturbation, expression validation, and in vitro pharmacologic evaluation. Integration converged on five genes (TRIM28, HNRNPH1, ARHGEF10L, C1RL, and UCHL3), with TRIM28 showing the highest feature importance and links to inflammatory, immune, metabolic, and proliferative programs. AKI exhibited intensified intercellular communication and an innate-skewed immune landscape. TRIM28 was robustly upregulated in HK-2 H/R and mouse RIRI kidneys and was also directly detected in the human urine proteome. In HK-2 cells, TRIM28 knockdown dampened, whereas overexpression amplified, IL-17–linked inflammatory signaling and apoptotic responses. Docking-prioritized HY-N10592 improved viability, reduced H/R-associated TRIM28 induction, IL-17–linked output, and apoptotic marker activation, and showed CETSA-supported cellular engagement of TRIM28. This integrative framework prioritizes TRIM28 as a candidate regulator linking tubular injury mechanisms with clinically relevant urinary signals and nominates HY-N10592 as a candidate chemical tool with CETSA-supported cellular target engagement for further mechanistic and in vivo evaluation in AKI.

Fluorescence-guided imaging has increasingly been integrated into robot-assisted urologic surgery to improve intraoperative visualization of vascular anatomy, tissue perfusion, lymphatic drainage, tumor-related landmarks, and reconstructive anatomy. However, the global research landscape, collaborative structure, intellectual foundation, and thematic evolution of fluorescence-guided robot-assisted urologic surgery have not been systematically characterized. In this study, publications related to fluorescence-guided robot-assisted urologic surgery were retrieved from the Web of Science Core Collection from 1998 to May 16, 2026. After screening, 457 English-language articles and reviews were included. CiteSpace, VOSviewer, and the bibliometrix package in R were used to analyze annual publication trends, countries/regions, institutions, authors, journals, cited journals, co-cited references, keyword co-occurrence, burst terms, trend topics, and thematic evolution. Publication output remained limited before 2011, increased gradually thereafter, and expanded more rapidly after 2018, with peak outputs in 2024 and 2025. The United States, Italy, and the Netherlands were the leading contributors, while Leiden University, Leiden University Medical Center, the Netherlands Cancer Institute, and Cleveland Clinic Foundation represented major institutional hubs. Co-cited references and keyword analyses showed that the knowledge base of this field is mainly organized around indocyanine green-guided robotic partial nephrectomy, fluorescence-enhanced radical prostatectomy, sentinel lymph node mapping, and robot-assisted ureteral reconstruction. “Indocyanine green,” “robotic surgery,” “prostate cancer,” “image-guided surgery,” “partial nephrectomy,” “radical prostatectomy,” and “augmented reality” were major conceptual themes. Recent hotspots included near-infrared fluorescence, ureteral stricture, lymph node dissection, positive surgical margins, artificial intelligence, and navigation. Overall, fluorescence-guided robot-assisted urologic surgery is evolving from early feasibility exploration toward procedure-specific clinical application, reconstructive precision, oncologic safety assessment, and digitally integrated surgical navigation. Future studies should emphasize standardized fluorescence protocols, quantitative imaging assessment, prospective multicenter validation, long-term clinical outcomes, and integration with artificial intelligence, augmented reality, and molecular imaging. Because bibliometric indicators reflect research activity and citation relationships rather than direct clinical efficacy or patient benefit, these findings should be interpreted as a map of research development and evidence gaps rather than as evidence supporting the superiority of fluorescence-guided robotic surgery.

Background: Renal ischemia-reperfusion injury (RIRI) is a major cause of acute kidney injury (AKI) and contributes to delayed graft function and progression toward chronic kidney disease. In addition to oxidative stress and inflammation, RIRI induces profound metabolic derangements, particularly suppression of tubular fatty-acid β-oxidation (FAO), leading to energetic stress, lipid accumulation, and maladaptive repair. Peroxisome proliferator-activated receptor-α (PPARα) is a key regulator of tubular FAO, but whether Schisandrin B (Sch B) mitigates RIRI through restoration of a PPARα-associated metabolic program remains unclear. Objective: To determine whether Sch B alleviates RIRI in association with restoration of tubular FAO and attenuation of lipid accumulation and fibrotic remodeling. Methods: A unilateral murine renal I/R model and an HK-2 hypoxia/reoxygenation (H/R) model were used. Mice received Sch B (20 or 40 mg/kg/day) before I/R, and a subset was co-treated with the PPARα antagonist GW6471. Renal function, tubular injury, fibrosis, lipid accumulation, and FAO-related proteins were assessed by serum biochemistry, histopathology, Oil Red O staining, transmission electron microscopy, immunohistochemistry, immunofluorescence, and Western blotting. Bulk RNA-seq and public single-cell RNA-seq datasets were integrated to characterize metabolic pathway remodeling and cell-type-associated PPARα changes. Molecular docking and molecular dynamics simulations were performed to explore the potential interaction between Sch B and PPARα. Results: Sch B significantly improved renal function, reduced tubular injury, and attenuated interstitial collagen deposition after I/R. Sch B also reduced lipid droplet accumulation, preserved mitochondrial ultrastructure, and restored the expression of FAO-related proteins, including CPT1A, CPT2, and ACADM. In vivo and in vitro, Sch B decreased α-SMA, COL1A1, and vimentin expression, indicating attenuation of EMT-associated/profibrotic remodeling. Integrated transcriptomic analyses supported marked metabolic reprogramming after I/R, with enrichment of FAO- and PPAR-related pathways and reduced PPARα expression predominantly in tubular compartments. Sch B was associated with restoration of tubular PPARα expression, while docking and molecular dynamics analyses supported a plausible Sch B-PPARα interaction in silico. GW6471 blunted the beneficial effects of Sch B on fibrosis-related and FAO-related readouts. Conclusions: Sch B alleviates RIRI and limits subsequent fibrotic remodeling in association with restoration of a PPARα-related tubular FAO program, reduced lipid accumulation, and preservation of tubular metabolic homeostasis. These findings identify metabolic reprogramming as an important component of Sch B-mediated renoprotection, although the precise mode by which Sch B regulates PPARα requires further investigation.

Manganese (Mn) is an essential trace element, but increasing industrial and agricultural use has led to elevated levels of environmental Mn levels. Chronic overexposure to Mn can cause a Parkinson's-like neurodegenerative disorder; however, the underlying mechanisms remain incompletely understood. This study combined in vitro and in vivo models to investigate the role of the cGAS-STING/NLRP3 axis in regulating the p38 MAPK/NF-κB pathway in the process of Mn-induced Tau aggregation leading to neurotoxicity. Our results demonstrated that MnCl2 exposure significantly activated both the cGAS-STING/NLRP3 signaling axis and the p38 MAPK/NF-κB pathway, accompanied by increased Tau expression. Genetic ablation of cGAS, STING, or NLRP3 attenuated Mn-induced Tau upregulation, indicating that the cGAS-STING/NLRP3 signaling axis mediates Tau expression. RNA-seq analysis further revealed that the decreased Tau expression in knockout cells is associated with the MAPK/NF-κB signaling pathway. Pharmacological inhibition of p38 MAPK or NF-κB markedly downregulated cGAS-STING signaling, inflammatory cytokine release, and phosphorylated Tau (p-Tau) levels. Moreover, we observed colocalization and interaction among p-p38, p-p65, and p-Tau. Overall, these findings reveal that Mn activates the cGAS-STING/NLRP3 signaling axis regulated by the p38 MAPK/NF-κB pathway, driving pathological Tau aggregation.

The widespread application of nanomaterials raises increasing concerns about their inhalation-induced pulmonary toxicity. Emerging evidence highlights that epigenetic regulation plays a critical role in mediating these effects. This review synthesizes key epigenetic mechanisms involved, including DNA methylation, histone acetylation, and noncoding RNA regulation. Nanomaterials induce bidirectional DNA methylation patterns-global hypomethylation alongside promoter-specific hypermethylation-primarily through oxidative stress and metal ion interference. Histone acetylation, governed by the balance between histone acetyltransferases and deacetylases, is frequently disrupted, leading to aberrant chromatin structure and altered gene expression. Noncoding RNAs form complex regulatory networks that modulate inflammation and fibrosis, whereas the potential involvement of chromatin remodeling remains largely unexplored in nanomaterial-induced pulmonary toxicity, warranting further investigation. Collectively, these epigenetic alterations drive the onset and progression of nanomaterial-induced pulmonary diseases, providing a theoretical foundation for epigenetic-based intervention strategies and risk assessment.

Robot-assisted ureteral reconstruction has evolved from bowel substitution to free oral mucosal grafts and vascularized appendiceal techniques, yet the intellectual structure and clinical maturity of these autologous tissue strategies remain unclear. PubMed and the Web of Science Core Collection were searched from inception through 2 August 2026. Records were merged, deduplicated, screened, and linked to OpenAlex for bibliometric enrichment. Publication trends, institutional contributions, co-citation patterns, thematic evolution, evidence maturity, and outcome reporting were assessed. Among 201 unique records screened, 74 publications were included in the bibliometric corpus and 66 primary clinical or technical reports formed the evidence-maturity subset. Bowel segments were the largest category (28/74), followed by buccal mucosa (22/74), appendix (12/74), lingual/labial mucosa (11/74), and mixed tissue (1/74). Thirty-six publications appeared during 2024–2026, and co-citation analysis identified distinct mucosal-graft and bowel-substitution foundations. Of the 66 primary reports, 24 were classified as E1, 8 as E2, 10 as E3, 22 as E4, and 2 as E5. Outcome reporting remained heterogeneous, device-free status was not explicitly detectable, while patient-reported outcomes appeared in only 4–17

Robot-assisted partial nephrectomy (RAPN) is an important nephron-sparing approach for renal tumors, with increasing emphasis on postoperative renal functional preservation. Preservation of renal function is clinically relevant in patients with reduced renal reserve or factors associated with future renal decline. However, the global research landscape and emerging trends in this field remain unclear. This study performed a bibliometric analysis of publications related to robot-assisted partial nephrectomy and renal function preservation, with emphasis on functional outcomes and CKD-related concepts identified within the literature. Publications from 2008 to 2026 were retrieved from the Web of Science Core Collection on May 10, 2026. Only English-language articles and reviews were included. Data were analyzed using Excel, VOSviewer, CiteSpace, Charticulator, and Scimago Graphica. A total of 276 publications were included, comprising 245 articles and 31 reviews. Publication output showed steady growth, with peaks in 2017 and 2022. Urology and nephrology were the dominant category. The United States led in publications, citations, and H-index, followed by Italy and China, with collaboration centered mainly on the United States and Italy. Cleveland Clinic and Temple University were leading institutions. Keyword analysis identified partial nephrectomy, ischemia, warm ischemia time, eGFR, small renal mass, and trifecta as major themes. The field has evolved from technical exploration toward ischemia reduction, nephron preservation, standardized outcome reporting, and individualized risk stratification. Future studies should prioritize prospective multicenter designs and standardized renal functional endpoints.

TRIM47 is an emerging E3 ubiquitin ligase of the tripartite motif family that has been increasingly implicated in inflammation, tissue injury, fibrosis, and cancer. Rather than acting as a disease-specific factor, TRIM47 appears to function as a context-dependent organizer of ubiquitin signaling, in which substrate selection and ubiquitin-chain topology shape distinct pathological outputs. Through K48-linked ubiquitination, TRIM47 promotes degradation of inhibitory or protective proteins, including CYLD, SIRT1, PPM1A, FBP1, CDO1, p53, Smad4, and XAF1, whereas through K63-linked ubiquitination it enhances signaling activity of mediators such as NEMO and PARP1. These substrate- and chain-dependent actions converge on a limited set of recurrent mechanisms, including inflammatory amplification, profibrotic remodeling, metabolic reprogramming, ferroptosis resistance, apoptosis escape, and DNA repair rewiring. This framework helps explain the repeated involvement of TRIM47 across innate immune dysregulation, organ injury, fibrogenesis, tumor progression, and treatment response. Notably, TRIM47 may also act as a double-edged regulator of therapy, promoting resistance to platinum-, taxane-, and endocrine-based treatments while potentially increasing vulnerability to PARP inhibition in selected homologous recombination-deficient settings. Although these observations support TRIM47 as a promising biomarker and therapeutic target, major gaps remain, including incomplete substrate and ubiquitin-site mapping, limited cell type-specific in vivo validation, insufficient structural and interactome data, and the lack of TRIM47-selective inhibitors. A mechanism-centered understanding of TRIM47 will be essential for improving disease stratification and developing rational TRIM47-directed therapies.

Nickel oxide nanoparticles (NiONPs) are known to induce pulmonary fibrosis and its mechanism remain incompletely understood. This study focused on the mechanism of hsa_circ_0007702-down-regulating miR-181d-5p mediated SLC7A11, then inhibited disulfidptosis and alleviated collagen deposition. We found that NiONPs led to the increasing SLC7A11, GLUT1, α-SMA, COL1A1 and the decreasing NOX4 expression in both rat pulmonary fibrosis and BEAS-2B collagen deposition models. Conversely, siRNA knockdown of SLC7A11 and inhibition of disulfidptosis decreased GLUT1, α-SMA and COL1A1 expression, increased NOX4, S and G2 phase fractions with more organized F-actin structures in BEAS-2B cells, suggesting that SLC7A11-mediating disulfidptosis alleviated NiONPs-induced collagen deposition. In addition, hsa_circ_0007702, a highly expressed circRNA in the lung, was upregulated when NiONPs was induced. hsa_circ_0007702 enhanced the expression of miR-181-5p and promoted disulfidptosis during NiONPs-induced. Furthermore, knockdown of hsa_circ_0007702 and lentivirus overexpressing miR-181d-5p decreased SLC7A11, GLUT1, α-SMA, COL1A1 expression, and increased miR-181d-5p, NOX4, S and G2 phase fractions with more organized F-actin structure, indicating that knockdown hsa_circ_0007702 up-regulating miR-181d-5p and down-regulating SLC7A11 inhibited disulfidptosis and alleviated collagen deposition. In summary, suppression of the disulfidptosis ameliorated NiONPs-induced collagen deposition by hsa_circ_0007702/miR-181d-5p/SLC7A11 axis. This study is the first to reveal the role of disulfidptosis in NiONPs induced collagen deposition. Our results reveal a novel mechanistic insight into noncoding RNA-based disulfidptosis and identify the hsa_circ_0007702/miR-181d-5p/SLC7A11 axis as a promising therapeutic target for pulmonary fibrosis.

Renal ischemia-reperfusion injury (RIRI) is characterized by a surge of oxidative stress, lipid peroxidation, and mitochondrial dysfunction, leading to ferroptotic tubular cell death and renal impairment. Recent findings implicate ZNRF2, a RING-type E3 ubiquitin ligase localized to the endo‑lysosomal membrane, as a central regulator that integrates ubiquitin-mediated signaling, ferroptosis susceptibility, and mitochondrial quality control (MQC) pathways. In this review, we synthesize current evidence on ZNRF2's structural features, ubiquitination targets (e.g., GPX4, SLC7A11, NCOA4), and its modulation of key MQC processes-DRP1-driven mitochondrial fission, PINK1-Parkin-mediated mitophagy, and lysosomal clearance via mTORC1/TFEB axis. We propose a temporal model aligning ischemia and reperfusion phases with specific redox and cell-death events, and highlight testable hypotheses such as ZNRF2's control over GPX4 stability or ferritinophagy dynamics. Moreover, we discuss therapeutic perspectives, including pharmacological modulators of ZNRF2 activity (small‑molecule stabilizers, PROTACs), and timing-based intervention windows. This integrated mechanistic framework advances understanding of RIRI pathogenesis and opens avenues for novel redox-targeted therapeutic strategies.

To compare perioperative and oncologic outcomes between single-port (SP) and multi-port (MP) retroperitoneal robotic-assisted partial nephrectomy (RAPN) in obese patients with renal tumors. A comprehensive literature search was conducted in PubMed, Embase, Scopus, and Web of Science up to July 2025. Eligible studies were those directly comparing SP-RAPN with MP-RAPN in obese patients (BMI ≥30 kg/m2). Extracted data included operative duration, intraoperative blood loss, warm ischemia time, length of hospitalization, complication rates, and oncologic outcomes, which were synthesized using RevMan 5.4. Three retrospective studies involving 694 patients (252 SP, 442 MP) were included. SP-RAPN was associated with a shorter hospital stay (WMD = −0.29 days, P = 0.02) but a longer warm ischemia time (WMD = 5.23 min, P < 0.00001). No significant differences were observed in operative time, estimated blood loss, complication rate, or positive surgical margins. The SP group had higher tumor complexity based on R.E.N.A.L. nephrometry scores. SP-RAPN demonstrates comparable safety and oncologic outcomes to MP-RAPN in obese patients, with the added benefit of reduced hospital stay. However, increased ischemia time should be considered when selecting the surgical approach. High-quality prospective trials are needed to confirm these findings.

Neurodegenerative diseases (NDDs) represent a rapidly escalating global health challenge, contributing significantly to the worldwide disease burden and posing substantial threats to public health systems across nations. Among the many risk factors for neurodegeneration, aging is the major risk factor. In the context of aging, multiple factors lead to the release of endogenous DNA (especially mitochondrial DNA, mtDNA), which is an important trigger for the activation of the cGAS-STING innate immune pathway. Recent studies have identified an increasing role for activation of the cGAS-STING signaling pathway as a driver of senescence-associated secretory phenotypes (SASPs) in aging and NDDs. The cGAS-STING pathway mediates the immune sensing of DNA and is a key driver of chronic inflammation and functional decline during the aging process. Blocking cGAS-STING signaling may reduce the inflammatory response by preventing mtDNA release and enhancing mitophagy. Targeted inhibition of the cGAS-STING pathway by biological macromolecules such as natural products shows promise in therapeutic strategies for age-related NDDs. This review aims to systematically and comprehensively introduces the role of the cGAS-STING pathway in age-related NDDs in the context of aging while revealing the molecular mechanisms of the cGAS-STING pathway and its downstream signaling pathways and to develop more targeted and effective therapeutic strategies for NDDs.

Background:Type 2 diabetes mellitus (T2DM) is a common comorbidity of chronic obstructive pulmonary disease (COPD), which significantly increases the risk of rehospitalization and mortality in patients with COPD. Therefore, the purpose of this study was to identify the influencing factors of COPD complicated by T2DM and to construct a visualized disease prediction model. Method:We included the medical records of 1,773 patients with COPD treated at Quzhou People's Hospital from 2020 to 2023. Subjects were randomly divided into a training set (n = 1,241) and a test set (n = 532) in a 7:3 ratio. Variable selection was performed using the least absolute shrinkage and selection operator (LASSO), Pearson correlation, and multicollinearity diagnostics. Variables were then refined through backward stepwise selection based on the Akaike Information Criterion (AIC) to construct a nomogram. The accuracy of the nomogram was evaluated using receiver operating characteristic (ROC) curves, calibration curves, and the Hosmer-Lemeshow test (H-L test). The clinical utility of the model was evaluated using decision analysis curves (DCA). Additionally, k-fold cross-validation (k = 10) was performed to rigorously assess model stability and mitigate the risk of overfitting. A sex-stratified subgroup analysis was also conducted to address potential sex-related bias. Results:The prevalence of T2DM in COPD patients was 27.13%. Seven independent predictors of COPD complicated by T2DM were identified: arterial partial pressure of carbon dioxide (PCO2) (OR = 1.04, 95%CI: 1.02-1.05), neutrophil number (NEUT) (OR = 1.15, 95%CI: 1.10-1.19), C-reactive protein (CRP) (OR = 1.01, 95%CI: 1.01-1.02), erythrocyte sedimentation rate (ESR) (OR = 1.03, 95%CI: 1.02-1.05), bilirubin (OR = 0.92, 95%CI: 0.88-0.96), triglyceride (TG) (OR = 1.33, 95%CI: 1.13-1.56), and body mass index (BMI) (OR = 1.16, 95%CI: 1.11-1.20). The model demonstrated good predictive performance, with a C-index of 0.78. The area under the curve (AUC) values were 0.79 (95%CI: 0.76-0.81) for the training set and 0.80 (95%CI: 0.76-0.84) for the test set, consistent with the k-fold cross-validation average AUC of 0.79 (95%CI: 0.76-0.81). Calibration curves and the H-L test (P >0.05) indicated good agreement between predicted and observed outcomes. DCA curves demonstrated clinical utility across threshold probabilities. Subgroup analysis showed robust performance in both male (0.82, 95%CI: 0.77-0.86) and female (0.71, 95%CI: 0.60-0.83) groups, with no significant difference in discriminatory ability (DeLong P = 0.101). Conclusion:In this study, we developed and internally validated a visualized prediction model for early identification of T2DM risk in patients with COPD. This tool may facilitate targeted prevention strategies by identifying high-risk populations. While the model demonstrated good performance, external validation is still required to confirm its generalizability.

BACKGROUND:Renal ischemia-reperfusion injury (RIRI) is a significant cause of acute kidney injury(AKI) and delayed graft function(DGF), impacting post-transplant outcomes. Mitochondrial dynamics, in particular fission and fusion, play a pivotal role in the cellular response to RIRI. The modulation of these dynamics represents a potential therapeutic target. Schisandrin B (Sch B), a component derived from traditional Chinese medicine, has shown protective roles in various organ injuries, but its effect on RIRI through mitochondrial dynamics remains unexplored. OBJECTIVE:This study explores the previously uninvestigated role of Sch B in modulating mitochondrial dynamics as a potential means of alleviating RIRI. By focusing on mitochondrial fission and fusion, this research provides novel insights into the therapeutic potential of Sch B, distinguishing it from existing approaches. METHODS:HK-2 cells were treated with hypoxia/reoxygenation (HR) in order to simulate renal ischemia-reperfusion injury (RIRI) in vitro. In vivo, mice underwent renal ischemia followed by reperfusion, which allowed for the simulation of the injury. Sch B's impact on mitochondrial dynamics, apoptosis, and oxidative stress was assessed through mitochondrial morphology assays, Western blotting for mitochondrial and apoptotic markers, TUNEL staining, and measurement of reactive oxygen species. Key molecular interactions were explored via Western blotting, molecular docking, SPR, and cellular thermal shift assays. In vivo, renal pathological damage was evaluated using HE, PAS, and TUNEL staining, while immunohistochemistry and immunofluorescence were employed to detect the expression levels of mitochondrial dynamics proteins and p-AKT1. RESULTS:First, we unveiled that Schisandrin B (Sch B) significantly mitigated oxidative stress and apoptosis in HK-2 cells subjected to hypoxia-reoxygenation conditions. Sch B pretreatment notably enhanced cell viability and mitochondrial function, demonstrating its superior antioxidant capabilities compared to NAC. Second, we discovered that Sch B's protective effects involve regulating mitochondrial dynamics by decreasing fission markers, such as DRP1, while increasing fusion proteins, including OPA1 and MFN2. Furthermore, our studies revealed that Sch B directly binds to AKT1, promoting its phosphorylation and localization to mitochondria, thereby enhancing mitochondrial resilience. Finally, we demonstrated that in vivo administration of Sch B reduced renal damage and apoptosis in mouse models of renal ischemia-reperfusion injury (RIRI), while immunohistochemical analyses unveiled its role in promoting mitochondrial fusion and reducing fission, marking a significant advancement in understanding Sch B's therapeutic potential in RIRI. CONCLUSION:Our findings demonstrate for the first time that Sch B directly interacts with AKT1 protein, enhancing its phosphorylation and promoting mitochondrial localization. This innovative mechanism reduces oxidative stress, apoptosis, and mitochondrial fission, highlighting Sch B's unique capability to modulate mitochondrial dynamics in RIRI. These results establish Sch B as a promising therapeutic agent, offering a new dimension in the management of RIRI by targeting mitochondrial health.

Environmental exposure to elevated manganese (Mn) levels is significantly associated with neurocognitive deficits, attracting widespread attention, yet its underlying mechanisms remain incompletely defined. Ferroptosis is recognized as a crucial contributor to cognitive impairments. Our study demonstrates that Mn exposure activates the cGAS-STING pathway, mediating reactive oxygen species (ROS) generation and subsequently inducing apoptosis and ferroptosis. Mechanistically, Mn-induced cGAS-STING activation promotes oxidative stress, characterized by increased ROS and malondialdehyde (MDA) production, alongside diminished glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities. Furthermore, this activated pathway triggers apoptosis by mediating ROS-dependent alterations in Bax/Bcl-2 expression and Cytochrome C (Cyt C) release from mitochondria. In addition, excessive activation of the cGAS-STING pathway drives ROS accumulation, which impairs iron homeostasis and induces ferroptosis by regulating the expression of solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), ferroptosis suppressor protein 1 (FSP1), dihydroorotate dehydrogenase (DHODH), and acyl-CoA synthetase long-chain family member 4 (ACSL4). Critically, inhibition of either the cGAS-STING pathway or ROS significantly ameliorated Mn-induced oxidative stress, apoptosis, and ferroptosis. Overall, these findings establish that cGAS-STING pathway activation mediates ROS production, leading to apoptosis and ferroptosis, as an essential mechanism of Mn neurotoxicity. Consequently, targeting the cGAS-STING pathway or ROS represents a promising therapeutic strategy for mitigating Mn neurotoxicity.

Objective:Prostate cancer is a major threat to global male health. This study uses bibliometric methods to analyze the dynamics and trends in prostate cancer screening research, with the aim of optimizing screening strategies and informing policy decisions. Methods:Utilizing the Web of Science Core Collection database, this study retrieved prostate cancer screening-related literature published between 2014 and 2024, totaling 5,409 articles. Data processing and analysis were conducted using CiteSpace and the Bibliometrix R package, including citation network analysis, co-word analysis, cluster analysis, and trend analysis. Results:The analysis revealed the following key findings: (1) Global literature on prostate cancer screening has grown annually, with the United States, Europe, and China leading research activity; (2) Research hotspots include the risks and benefits of prostate-specific antigen (PSA) testing, MRI-based screening technologies, and the use of molecular and genetic biomarkers; (3) Emerging technologies, such as machine learning and nanodiagnostic techniques, are enhancing diagnostic precision and reducing overdiagnosis; (4) Network analysis of collaborations reveals a shift toward transnational and interdisciplinary research, particularly in integrating biomedical and computer science to drive rapid advancements in screening technologies. Conclusion:This study confirms the ongoing vibrancy and technological advancement in the global field of prostate cancer screening research, emphasizing the trend towards precision medicine. Future development of prostate cancer screening strategies should focus on risk-adapted screening and the application of novel biomarkers to optimize screening outcomes and reduce unnecessary medical interventions.