Search Results (10,890)

The role of gut microbiota and intestinal dysbiosis in promoting inflammaging in chronic kidney disease (CKD) has been the focus of intense research over the last years. Some alterations at the phyla level, such as abundance of Proteobacteria and reduction in Firmicutes/Bacteroidites (F/B) ratio and saccarolytic populations, have been consistently reported in CKD. Other mechanisms include microbial translocation through a “leaky gut” and subsequent molecular mimicry, immune dysregulation (unbalance between T reg and Th17 subsets), and epigenetic interactions. Alterations of metabolic pathways and of bacterial metabolites, such as butyrate and other short chain fatty acids (SCFA), also appear to play a key role in modulating progression of CKD. On the other hand, microbiota-based therapy appears promising and includes diet, prebiotics, probiotics, synbiotics, postbiotics and fecal microbiota transplantation (FMT). Modulation of microbiota could correct critical alterations, such as F/B ratio and T reg/Th17 unbalance, blunting inflammaging and potentially reducing progression of CKD and cardiovascular disease. Despite current limitations, gut microbiota is emerging as a powerful environmental factor which could be harnessed to interfere with key mechanisms leading to inflammaging in CKD. Full article

Background and Objectives: Identifying regulatory genes that integrate epigenetic, transcriptional, immune, and non-coding RNA networks may improve prognostic stratification in hepatocellular carcinoma (HCC). ZBTB40 is a poorly characterized transcription factor whose clinical relevance and multi-layered regulatory role in HCC remain unclear. This study systematically investigated the prognostic significance, molecular regulatory networks, and toxicogenomic interactions of ZBTB40 in HCC. Materials and Methods: Comprehensive multi-omics analyses were conducted utilizing TCGA-HCC datasets and various public bioinformatics platforms. We systematically evaluated ZBTB40 expression patterns, survival outcomes, clinicopathological associations, DNA methylation status, immune cell infiltration, and competing endogenous RNA (ceRNA) networks. Additionally, chemical–gene interactions were analyzed using the Comparative Toxicogenomics Database (CTD). Results: ZBTB40 was significantly overexpressed in HCC, closely correlating with advanced clinicopathological features and poor survival outcomes. This upregulation was significantly associated with promoter hypomethylation. Furthermore, ZBTB40 expression was associated with specific immune infiltration patterns. A ZBTB40-centered ceRNA network identified key regulatory miRNAs, including miR-24-3p, miR-34a-5p, miR-132-3p, and miR-222-3p, along with prognostically relevant lncRNAs and circRNAs. CTD analysis identified 39 key chemical modulators of ZBTB40 (e.g., sorafenib, aflatoxin B1) and revealed RNF13 and CHD3 as functionally related genes sharing substantial chemical interaction profiles. Functional analyses suggested ZBTB40’s involvement in chromatin remodeling, the cell cycle, and immune-related pathways. Conclusions: ZBTB40 expression is associated with multi-layered molecular features involving epigenetic, post-transcriptional, immune-related, and toxicogenomic signatures in HCC. Full article

Interfacial defect passivation has emerged as a critical strategy for mitigating non-radiative recombination losses in inorganic perovskite solar cells (PSCs). However, the distinct chemical environments at the bottom (hole-transport layer) and top (electron-transport layer) interfaces demand passivation agents with tailored functionalities—a principle that remains largely underexplored. Herein, we systematically employed two organic ammonium iodide salts, phenylethylammonium iodide (PEAI) and 2-thiophenemethylammonium iodide (ThMI), to separately modulate the bottom NiO_x/CsPbI₂Br and top CsPbI₂Br/PCBM interfaces of inverted PSCs with a configuration of ITO/NiO_x/CsPbI₂Br/PCBM/BCP/Ag. We reveal different interfacial modulation effects: bottom-interface modification by both PEAI and ThMI dramatically improves the fill factor (FF), with PEAI delivering a more pronounced enhancement due to improved interfacial contact and reduced series resistance. However, top-interface passivation effectively boosts the open-circuit voltage (V_oc), where ThMI exhibits superior voltage elevation capability over PEAI by neutralizing undercoordinated Pb²⁺ defects via its thiophene moiety. Capitalizing on this complementary selectivity, we construct an asymmetric dual-interface passivation architecture with PEAI at the bottom and ThMI at the top (ITO/NiO_x/PEAI/CsPbI₂Br/ThMI/PCBM/BCP/Ag), which synergistically enhances both FF and V_oc. Consequently, the optimized PEAI/ThMI device achieves a champion power conversion efficiency (PCE) of 15.44%, with a V_oc of 1.15 V, a J_sc of 16.34 mA/cm², and an FF of 82.15%, significantly outperforming the control device (11.79%). This work establishes a rational design paradigm for interface-specific passivation in inverted inorganic PSCs, highlighting the importance of molecular functionality in addressing distinct interfacial recombination pathways. Full article

Glycogen synthase kinase 3 (GSK3/Shaggy-like) belongs to evolutionarily conserved serine/threonine protein kinases that regulate plant morphological development, multi-hormone crosstalk and adaptation to abiotic stresses. However, systematic genome-wide characterization of CmGSK3 is still absent in melon (Cucumis melo L.). This study identified six CmGSK3 members on a whole-genome level, unevenly distributed among four chromosomes. Combined phylogenetic and synteny profiling separated these six genes into four conserved subclades; orthologous links were discovered between melon, Arabidopsis, and rice, revealing evolutionary conservation between monocot and dicot crops. Prediction of promoter cis-regulatory motifs combined with transcriptome datasets suggested that CmGSK3 genes participate in hormone transduction and environmental stress adaptation. Quantitative real-time PCR further verified that exogenous brassinosteroid (BR) application dramatically induced transcriptional accumulation of CmSK21 and CmSK22. Heterologous overexpression of these two genes in wild-type Arabidopsis significantly lowered plant sensitivity to BR, confirming they may function as negative modulators of the BR signaling cascade. Collectively, CmGSK3 members coordinate multiple metabolic routes, dominated by BR-related signal transduction, to manipulate melon growth and stress adaptability. This study establishes the first systematic research on the melon GSK3 family and supplies elite candidate genes for molecular breeding targeting fruit quality and stress resistance improvement in melon. Full article

Aspartame is a widely used artificial sweetener, but its possible relationship with rheumatoid arthritis (RA) remains insufficiently understood. This study aimed to explore, rather than prove, potential molecular links between aspartame-related targets and RA-associated gene networks. Three public RA transcriptomic datasets (GSE55235, GSE55457, and GSE77298) from the Gene Expression Omnibus (GEO) database were integrated as discovery/training data. Because these datasets included different tissue origins, batch correction was used to reduce dataset-level technical variation, whereas tissue-origin-related biological variation was not assumed to be fully removable. After differential expression analysis, RA-associated differentially expressed genes (DEGs) were identified. The single-cell dataset GSE200815 was used for cell annotation and cellular expression visualization; because its comparator group consists of psoriatic arthritis (PsA) samples rather than healthy controls, single-cell results were interpreted as RA-vs-PsA observations and were not treated as disease-versus-healthy-control evidence. Potential targets of aspartame were retrieved from ChEMBL, SwissTargetPrediction, and the Similarity Ensemble Approach (SEA), and were intersected with RA-related DEGs to construct an aspartame-gene-RA regulatory network. Diagnostic models were developed using 113 machine-learning algorithm combinations to determine an optimal multigene model and its core genes. HLA-DRB1 was selected for exploratory scTenifoldKnk-based virtual knockout mainly because it was included in the optimal model and has a well-established role in RA immunogenetics; the single-cell analysis was used only to describe cellular distribution in the RA/PsA dataset. Molecular docking was then used to evaluate the possible interaction between aspartame and HLA-DRB1. Forty-four intersected genes linked the predicted aspartame targets with RA DEGs. The random forest plus partial least-squares generalized linear model (RF + plsRglm) identified 16 core genes. Network-level interpretation indicated that these genes were distributed across immune/antigen-processing, inflammatory-signaling, protease/extracellular-matrix-remodeling, adhesion, metabolic, and proliferation-related modules; therefore, HLA-DRB1 was treated as a prioritized immune-module candidate rather than as the sole driver of the network. Following virtual knockout of HLA-DRB1, affected genes were enriched in extracellular matrix organization, extracellular structure organization, extracellular matrix, collagen trimer, extracellular matrix structural constituent, and collagen binding. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways included integrin signaling, focal adhesion, proteoglycans in cancer, cytoskeleton in muscle, and phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling. Molecular docking showed a minimum binding energy of −6.7 kcal/mol, which was more negative than the preset stability criterion of −5.0 kcal/mol, and the docking pose suggested contacts around ARG-146. This integrative analysis suggests a hypothesis-generating association between aspartame-related predicted targets and RA-relevant molecular networks involving HLA-DRB1 and other core genes. The findings do not establish causality and require experimental, epidemiological, biophysical, and tissue-stratified validation before any causal or clinical inference can be made. Full article

Bolting time is a pivotal agronomic trait that determines the yield and commercial quality of Brassica rapa ssp. chinensis var. utilis. To investigate the molecular basis of early bolting, an early-bolting line ‘m662’ and a late-bolting line ‘t151’ were used in this study. Phenotypic evaluation combined with shoot apical meristem (SAM) observation showed that 10 days of low-temperature vernalization markedly accelerated bolting in ‘t151’. Subsequently, SAM samples from ‘m662’, non-vernalized ‘t151’, and 10-day vernalized ‘V10-t151’ were collected at five developmental stages (7, 10, 13, 16, and 19 d after transplanting) for transcriptome sequencing. Weighted gene co-expression network analysis revealed that key module genes related to gibberellin signaling were specifically enriched in ‘m662’ before bolting, whereas those in the middle and late bolting stages were enriched in hormone response, cell cycle regulation, and floral organ development. In ‘t151’, hub genes detected at 7–13 d included three paralogs of the floral integrator gene SOC1 and BraA06.FPF1. BrSOC1 (BraA03g024230.4C) was significantly upregulated in response to vernalization. DEGs identified during the late developmental stage (16–19 d) included genes involved in transmembrane transport processes, flower development, reproductive shoot system development. Expression analysis across the three materials showed that vernalization accelerated bolting in ‘t151’ by repressing BrFLC expression and promoting BrSOC1 expression. This study elucidates the dynamic transcriptomic network underlying early bolting in non-heading Chinese cabbage, providing key functional genes and mechanistic insights for bolting regulation and molecular breeding. Full article

Mycobacterium abscessus subsp. massiliense (Mabs) is an emerging nontuberculous mycobacterium associated with difficult-to-treat infections due to intrinsic antimicrobial resistance, intracellular persistence, biofilm formation, and limited responsiveness to currently available therapeutic regimens. In this context, adjuvant strategies targeting iron-dependent metabolic pathways and metal homeostasis may enhance the efficacy of conventional antimicrobials. This study investigated deferoxamine (DFO), a clinically approved iron chelator, as a potential adjuvant against Mabs using integrated in vitro and in silico approaches. Cytocompatibility was assessed using an MTT assay in RAW 264.7 macrophages and a hemolysis assay in human erythrocytes. Antimicrobial activity was evaluated through minimum inhibitory concentration (MIC) and minimum bactericidal concentration (MBC) assays, while interactions with clarithromycin (CLA) and amikacin (AMK) were assessed using the checkerboard method. Effects on virulence-associated phenotypes were examined through biofilm formation assays and protein quantification in extracellular vesicle-enriched fractions. Intracellular activity and modulation of inflammatory mediator gene expression were investigated in Mabs-infected RAW 264.7 macrophages through colony-forming unit (CFU) recovery and reverse transcription quantitative polymerase chain reaction (qPCR). DFO exhibited low cytotoxicity and negligible hemolytic activity under the tested conditions. Direct antimicrobial testing revealed a predominantly bacteriostatic profile (MIC = 9.75 µg/mL; MBC > 10 mg/mL), whereas checkerboard analysis suggested a synergistic interaction with CLA (FICI = 0.047), which requires further confirmation by time-kill or CFU-based combination assays. Furthermore, DFO reduced biofilm biomass, decreased protein levels in vesicle-enriched fractions, lowered intracellular bacterial burden, and modulated cytokine gene expression in infected macrophages. Molecular docking, ADME/Tox, and PASS analyses generated exploratory hypotheses regarding potential molecular interactions and pharmacological properties. Overall, these findings support DFO as a promising experimental adjuvant candidate for further investigation against Mabs, particularly in combination with clarithromycin. However, confirmation of a putative iron-restriction-associated mechanism and its translational relevance will require validation in additional clinical isolates, iron-rescue experiments, mature biofilm models, and in vivo studies. Full article

Conventional photothermal therapy often relies on high-intensity laser excitation due to the limited photothermal conversion efficiency (PCE) of existing photothermal agents (PTAs), which compromises treatment safety and restricts clinical translation. To address this limitation, we designed and synthesized a series of boron-dipyrromethene (BODIPY)-based derivatives (BDP 1–4) featuring gradient-enhanced donor–acceptor (D-A) push–pull electronic effects for efficient photothermal antitumor therapy. The structure–activity relationships were systematically elucidated through photophysical characterization and in vitro/in vivo photobiological evaluation. From BDP 1 to BDP 4, the progressively strengthened push–pull effect leads to enhanced intramolecular charge transfer (ICT), which, in turn, results in a narrowed HOMO-LUMO gap, redshifted absorption into the near-infrared (NIR) region (up to 843 nm), markedly attenuated fluorescence emission, and a remarkable increase in PCE up to 88.3%. To improve water dispersibility and tumor targeting, these molecules were further encapsulated into nanoparticles using DSPE-PEG₂₀₀₀, and the nanoformulations retained high PCE. Both in vitro and in vivo studies demonstrated that under low-power laser irradiation (0.5 W·cm⁻², 808 nm), the nanoformulation of BDP 4, which exhibited the highest PCE among the series, achieved pronounced photothermal tumor ablation without inducing systemic toxicity. Overall, this study proposes a molecular design strategy that synergistically modulates NIR absorption and photothermal conversion by enhancing the D-A push–pull effect. This strategy provides a design rationale for developing efficient, low-toxicity organic PTAs, and demonstrates potential applicability in low-power PTT modalities. Full article

Osteoarthritis (OA) is a chronic, debilitating degenerative joint disease whose prevalence is rising markedly with the rapid aging of the global population. In this study, we investigated the chondroprotective efficacy of NP-2007, an enzymatically hydrolyzed low-molecular-weight collagen from Cervi cornu, using IL-1β-stimulated SW1353 human chondrocyte cells and a medial meniscal transection (MMT)-induced OA rat model. In SW1353 cells, NP-2007 considerably suppressed the expression of inflammatory mediators (iNOS, COX-2) and cytokines (TNF-α, IL-6) without cytotoxicity. Crucially, it restored matrix homeostasis by downregulating catabolic enzymes (MMP-3, MMP-13, and ADAMTS-5) and upregulating anabolic markers (COL2A1, aggrecan), a process associated with the modulation of the Wnt/β-catenin and phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathways and the recovery of the master chondrogenic factor SOX9. These in vitro findings were consistent with the in vivo results from the MMT model, where oral administration of NP-2007 (50 and 200 mg/kg) for 8 weeks effectively preserved articular cartilage structure and proteoglycan content while markedly reducing serum levels of catabolic biomarkers, including MMP-13 and COMP. Collectively, our findings demonstrate that NP-2007 exerts potent chondroprotective effects by modulating the balance between cartilage degradation and synthesis, suggesting its potential as a therapeutic candidate for the management of OA. Full article

Radiation therapy is a fundamental pillar in cancer treatment, yet its clinical efficacy is frequently compromised by the development of intrinsic and acquired tumor radioresistance. This review provides a comprehensive analysis of the molecular mechanisms underlying radioresistance, with a specific focus on the Epithelial–Mesenchymal Transition (EMT) and its regulation by microRNAs (miRNAs). EMT is recognized as a key driver of therapeutic resistance, enabling cancer cells to acquire enhanced migratory capacity, stem-like characteristics, and resistance to apoptosis. Importantly, ionizing radiation can itself function as a cellular stressor that induces EMT through major signaling pathways, including TGF-β, Wnt, and Notch, thereby establishing a self-reinforcing loop that promotes resistance. In addition, this review highlights the pivotal role of miRNAs as post-transcriptional regulators within this network. Dysregulated miRNAs, acting as either tumor suppressors or oncogenes, modulate EMT-transcription factors and DNA damage repair pathways to influence cellular radiosensitivity. The complex interplay between these factors and the tumor microenvironment is also explored. Finally, emerging therapeutic strategies designed to break this resistance loop, such as EMT inhibitors, miRNA mimics, and antagomirs, as well as combination therapies, are evaluated. Collectively, these approaches hold significant promise for restoring radiosensitivity and improving clinical outcomes in precision oncology. Full article

Regionally, compound agroecological stress arising from both natural and anthropogenic emergy inputs may influence maize transcriptomic responses; however, evidence across multiple scales remains limited. We developed a reproducible five-step framework integrating a macro-level compound stress index, molecular response modules, cross-scale coupling, spatial continuity, and independent field validation. Nine variables (emergy indicators ELR, Fn, and NEYR; climate; soil; and terrain) were PCA-weighted into a Composite Abiotic Stress Intensity Index (CASI; first three PCs = 83.7%; and prefecture-level Moran’s I = 0.463). Across 15 public RNA-seq datasets (286 samples), WGCNA identified five separable modules (drought–heat, reproductive stage heat, low nitrogen/phosphorus, osmotic salt, and chronic compound), 270 core genes, and four cross-module hubs (ZmDREB2A, ZmHSFA2, ZmWRKY33, and ZmNRT2.1). With n = 21, the sCCA (r₁ = 0.81, permutation p = 0.003; LOO-CV r = 0.71), random forest, and spatial error model all confirmed coupling between ELR and the drought–heat module (β = 0.51, p = 0.008). PLS-DA four-zone partitioning (Q² = 0.548) and a county-level second-order trend surface (R² = 0.67) verified spatial continuity. GSVA on five independent field RNA-seq datasets yielded 74.4 to 82.8% core gene directional consistency and Cliff’s δ of 0.59 to 0.68 (large effect), avoiding circular reasoning. The framework enables molecular analysis for precision agriculture and climate-resilient breeding. Full article

Camel milk is increasingly recognized as a premium functional food, attributed to its rich nutraceutical compounds. Recent research has concentrated on the nanoscale extracellular vesicles derived from camel milk (CM-EVs), which exhibit distinctive properties. This review examines the methodologies for isolating and characterizing CM-EVs, alongside their potential health benefits in functional foods and nutraceuticals. CM-EVs have the capacity to safeguard functional proteins, noncoding RNAs, and bioactive lipids from degradation within the gastrointestinal tract, rendering them particularly suitable for incorporation into infant formulas, adult dietary supplements, and nutraceuticals targeting chronic inflammatory and metabolic disorders. Preclinical models indicate that CM-EVs can mitigate oxidative stress, enhance intestinal barrier integrity, and modulate gut microbiota, thereby contributing to the reduction in colonic injury and inflammation. Nonetheless, the majority of these findings are derived from laboratory and animal studies, highlighting a substantial deficiency in human clinical trials. Critical research gaps remain, necessitating further investigation into the elucidation of molecular mechanisms, assessment of long-term safety, evaluation of bioavailability, and compatibility with dairy processing techniques. This review underscores the significance of CM-EVs as bioactive food components and delineates research priorities, such as standardizing isolation methods, investigating food matrix integration, and providing translational evidence for their application in nutrition and preventive medicine. Full article

In patients with myocardial infarction (MI), the level of sphingolipids, such as ceramide (Cer), is elevated and is associated with an increased risk of progression towards heart failure (HF). Dihydroceramide desaturase 1 (DES1) catalyses the conversion of dihydroceramide (dhCer) into Cer in the de novo sphingolipid pathway. While pharmacological inhibition of DES1 has shown therapeutic benefits in metabolic disease and cancer models, its role in cardiac remodelling remains unclear. This study aimed to determine whether pharmacological inhibition of DES1 using the novel compound, CIN038, attenuates cardiac remodelling following ischemia–reperfusion (I/R) injury. Three-month-old male C57Bl/6 mice underwent I/R or sham surgery (n = 8) and were treated with vehicle or CIN038 (50 mg/kg/day, i.p.) for 28 days. Cardiac function, molecular changes, and lipid profiles in circulation and liver were assessed at the endpoint. CIN038 reduced infarct size and cardiac myocyte hypertrophy compared to the I/R + vehicle group. Profibrotic signalling was reduced in the infarcted hearts, as evidenced by reduced expression of Col1a1, Col3a1, and Tgfb mRNA and decreased levels of α-SMA and TGFβ1 protein expression. Inflammatory signalling was attenuated with reduced ERK and NFkB phosphorylation and suppression of Il-6-STAT axis. Despite these structural and molecular improvements, no changes were observed in cardiac function. Lipidomic analysis revealed selective alterations in circulating and hepatic lipid species, including plasmalogen phosphatidylethanolamines and ether-linked triglycerides, suggesting modulation of lipid metabolism. Collectively, these findings indicate that CIN038 attenuates post-ischemic cardiac remodelling by suppressing inflammatory and profibrotic signalling, highlighting DES1 as a potential therapeutic target following MI. Full article

Endoplasmic reticulum (ER) stress is a common state of cellular adversity experienced by tumor cells under unfavorable conditions such as hypoxia, nutrient deprivation, and oncogene activation. As the most conserved signaling branch of the unfolded protein response (UPR), the inositol-requiring enzyme 1α (IRE1α)- X-box-binding protein 1 (XBP1) pathway plays a central role in sustaining tumor cell survival, driving malignant progression, and remodeling the tumor microenvironment (TME). XBP1, the terminal transcription factor of this pathway, finely orchestrates tumor cell fate through both its canonical and non-canonical functions. This review systematically summarizes the dual mechanisms of XBP1 in cancer: within cancer cells, XBP1 promotes proliferation, metastasis, and chemoresistance via metabolic reprogramming, anti-apoptotic proteins, and DNA repair; within immune cells (macrophages, dendritic cells, T cells), XBP1 fosters an immunosuppressive microenvironment, while also modulating cancer-associated fibroblasts, endothelial cells, and osteoclasts. Despite its therapeutic promise, several major unresolved questions remain, including the precise molecular switch governing XBP1’s pro-tumorigenic versus anti-tumorigenic functions, the functional divergence between XBP1u and XBP1s isoforms in different cellular contexts, and the lack of reliable predictive biomarkers for patient stratification. Key translational challenges involve the on-target toxicity of systemic XBP1/IRE1α inhibition due to its essential roles in normal tissues, the cell-type-specific and context-dependent effects that complicate therapeutic outcomes, and the limited selectivity and off-target effects of current inhibitors, as well as compensatory activation of other UPR branches that may drive adaptive resistance. Finally, this review discusses XBP1-targeted therapeutic strategies, including small-molecule inhibitors, nucleic acid-based drugs, immunotherapeutic combination approaches, and XBP1-based tumor vaccines, and provides perspectives on future research directions, aiming to establish a theoretical foundation for the development of more effective and precise XBP1-targeted therapies for tumorigenesis and cancer progression. Full article

Cadmium (Cd) is an environmental nephrotoxicant that preferentially accumulates in the kidney and disrupts redox and energy metabolism. However, the protective effect of berberine (Ber) against Cd-induced nephrotoxicity remains insufficiently characterized. In the present study, male C57BL/6 mice were orally exposed to CdSO₄ (30 mg/kg body weight/day) for 30 days in the absence or presence of berberine (25 or 100 mg/kg/day). Renal function, histopathology, oxidative stress parameters, LC–MS/MS-based metabolomic profiling, gene and protein expression, and in silico ligand–target interactions were evaluated. Cd exposure markedly increased serum CREA, renal index, renal LDH activity, and MDA content, decreased SOD and CAT activities, and induced pronounced renal histopathological lesions. Ber significantly attenuated these abnormalities in a dose-dependent manner. Metabolomic analysis revealed that Cd broadly suppressed pyruvate metabolism, tricarboxylic acid cycle intermediates, and NAD+/NADH homeostasis, whereas berberine restored the levels of pyruvate, acetyl-CoA, oxaloacetate, citrate, isocitrate, succinate, fumarate, malate, NAD+, and NADH. In parallel, berberine normalized the expression of metabolism-related genes including the downregulation of Ldha and the upregulation of Cs, Sucnr1, G6pc, and Pfkm, with the high-dose regimen showing the most evident recovery. Western blotting further verified the lower LDHA protein expression after berberine treatment. Molecular docking demonstrated favorable potential berberine–LDHA binding, and molecular dynamics simulation supported the stability of the ligand–protein complex. Collectively, these findings indicate that berberine ameliorates Cd-induced renal injury, an effect that correlates with attenuated oxidative stress, modulation of LDHA-associated glycolytic pathways, and restoration of mitochondrial TCA-cycle activity and redox balance, highlighting berberine as a promising candidate for the prevention of heavy metal-associated nephrotoxicity. Full article