Search Results (292)

Air pollution acts as a pervasive oxidative stressor, disrupting global crop production and ecosystem health through the overproduction of reactive oxygen species (ROS). Hazardous pollutants impair critical physiological processes—photosynthesis, respiration, and nutrient uptake—triggering oxidative damage and yield losses. This review synthesizes current knowledge on plant defense mechanisms, emphasizing the integration of enzymatic (SOD, POD, CAT, APX, GPX, GR) and non-enzymatic (polyphenols, glutathione, ascorbate, phytochelatins) antioxidant systems to scavenge ROS and maintain redox homeostasis. We highlight the pivotal roles of transcription factors (MYB, WRKY, NAC) in orchestrating stress-responsive gene networks, alongside MAPK and phytohormone signaling (salicylic acid, jasmonic acid, ethylene), in mitigating oxidative stress. Secondary metabolites (flavonoids, lignin, terpenoids) are examined as biochemical shields against ROS and pollutant toxicity, with evidence from transcriptomic and metabolomic studies revealing their biosynthetic regulation. Furthermore, we explore biotechnological strategies to enhance antioxidant capacity, including overexpression of ROS-scavenging genes (e.g., TaCAT3) and engineering of phenolic pathways. By addressing gaps in understanding combined stress responses, this review provides a roadmap for developing resilient crops through antioxidant-focused interventions, ensuring sustainability in polluted environments. Full article

Auxin (IAA), a key natural signaling molecule, plays a pivotal role in regulating plant growth, development, and stress responses. Understanding its signal transduction mechanisms is crucial for improving crop yields. In this study, we conducted a comparative transcriptome analysis of wheat leaf and root tissues treated with different concentrations of IAA (0, 1, and 50 μM). Functional enrichment analysis revealed that differentially expressed genes (DEGs) exhibited tissue-specific regulatory patterns in response to auxin. Weighted Gene Co-expression Network Analysis (WGCNA) identified receptor-like kinase genes within the MEgreen module as highly correlated with auxin response, suggesting their involvement in both root and leaf regulation. Among them, TaPBL7-2B, a receptor-like kinase gene significantly upregulated under 50 μM IAA treatment, was selected for functional validation. Ectopic overexpression of TaPBL7-2B in Arabidopsis thaliana (Col-0) enhanced auxin sensitivity and inhibited plant growth by suppressing root development and leaf expansion. In contrast, knockout of the Arabidopsis homolog AtPBL7 reduced auxin sensitivity and promoted both root and leaf growth. Transcriptome analysis of Col-0, the TaPBL7-2B overexpression line, and the pbl7 mutant indicated that TaPBL7-2B primarily functions through the MAPK signaling pathway and plant hormone signal transduction pathway. Furthermore, qRT-PCR analysis of wheat varieties with differing auxin sensitivities confirmed a positive correlation between TaPBL7-2B expression and auxin response. In conclusion, TaPBL7-2B acts as a negative regulator of plant growth, affecting root development and leaf expansion in both Arabidopsis and wheat. These findings enhance our understanding of auxin signaling and provide new insights for optimizing crop architecture and productivity. Full article

Cadmium (CAD) is a prevalent environmental contaminant that poses serious cardiotoxic risks. The heart, kidney, liver, and brain are just a few of the essential organs that can sustain serious harm from CAD, a very poisonous heavy metal. The cardiotoxic mechanism of CAD is linked to oxidative damage and inflammation. A trace element with anti-inflammatory, anti-apoptotic, and antioxidant qualities, selenium (SEL) can be taken as a dietary supplement. The biotoxicity of heavy metal CAD is significantly inhibited by SEL, a mineral that is vital to human and animal nutrition. Through ROS-induced PARP-1/ADPR/TRPM2 pathways, this study seeks to assess the preventive benefits of selenium against cardiovascular damage caused by CAD. The SEL showed encouraging results in reducing inflammatory and oxidative reactions. Rats were given 0.5 mg/kg SEL and 3 mg/kg 2-Aminoethyl diphenylborinate (2-APB) intraperitoneally for five days, in addition to 25 mg/kg CAD given via gavage. Histopathological examination findings revealed that the morphologic changes in the hearts of the CAD group rats were characterised by marked necrosis and the degeneration of myocytes and congestion of vessels. Compared to the rats in the CAD group, the hearts of the SEL, 2-APB and SEL+2-APB groups showed fewer morphological alterations. Moreover, in rats given CAD, there was an increase in cardiac malondialdehyde (MDA), total oxidant (TOS), reactive oxygen species (ROS), caspase (Casp-3-9), and TNF-α, whereas glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and total antioxidant (TAS) decreased. SEL improved antioxidants, avoided tissue damage, and reduced cardiac MDA, TOS, and ROS. In rats given CAD, SEL decreased cardiac PARP-1, TRPM2, TNF-α, and caspase. In summary, by reducing oxidative stress and cardiac damage and modifying the ROS/PARP-1/TRPM2 pathway, SEL protected against CAD cardiotoxicity. Full article

In this study we searched for correlations between polymorphic variants that determine sex hormone-binding globulin concentration (SHBG_con) and uterine fibroids (UFs). The work was performed on a sample of 1542 women (569 with UFs and 973 without UFs [control]), from whom we obtained experimental data on the distribution of nine single-nucleotide polymorphisms (SNPs) affecting the SHBG_con (data confirmed in genome-wide association studies [GWASs]). When searching for associations with UFs, both the independent effects of SNPs and the effects of their SNP–SNP interactions (SNP-SNP_ints) were taken into account during the “deep study” of the functionality of seven important UF loci and 115 strongly linked [r² ≥ 0.80] variants (an in silico methodology was used). As the results show, two SHBG_con-related SNPs correlated with UF risk: rs3779195 [T/A] BAIAP2L1 (OR_AA = 0.38; 95%CI_AA = 0.20–0.91; p_perm(AA) = 0.023) and rs440837 [A/G] ZBTB10 (OR_GG = 1.93; 95%CI_GG = 1.17–3.14; p_perm(GG) = 0.010). At the same time, seven SHBG_con-related SNPs interacting with each other (four models of such SNP-SNP_ints [p_perm ≤ 0.01)] were found to influence UF risk. These SHBG_con-related SNPs, determining susceptibility to UF, showed strong functional relevance and were involved in pathways of gene transcription regulation, interactions with hormone ligand-binding receptors, the content control of SHBG, testosterone, liver enzymes, lipids, etc. This study’s results demonstrate the effect of significant SHBG_con-related genetic determinants of UF risk. Full article

Background/Objectives: Prostate cancer (PCa) is diagnosed at an earlier median age, more advanced stage, and has worse clinical outcomes in African American (AA) men compared to European Americans (EA). Methods: To investigate the role of aberrant DNA methylation in tumor-adjacent stroma (TAS), methyl binding domain sequencing (MBD-seq) was performed on AA (n = 17) and EA (n = 15) PCa patients. This was independently confirmed using the long interspersed nuclear element-1 (LINE-1) assay. Pathway analysis was performed on statistically significantly differentially methylated genes for AA and EA TAS. DNA methylation profiles of primary cultured AA and EA carcinoma-associated fibroblasts (CAFs) were compared with AA and EA TAS. AA and EA CAFs were treated with demethylating agent 5-Azacytidine (5-AzaC). Results: AA TAS exhibited higher global DNA methylation than EA TAS (p-value < 0.001). Of the 3268 differentially methylated regions identified (DMRs, p-value < 0.05), 85% (2787 DMRs) showed increased DNA methylation in AA TAS, comprising 1648 genes, of which 1379 were protein-coding genes. Based on DNA methylation levels, two AA subgroups were identified. Notably, AA patients with higher DNA methylation were predominantly those with higher Gleason scores. Pathway analysis linked methylated genes in AA TAS to several key signaling pathways (p-value < 0.05), including immune response (e.g., IL-1, IL-15, IL-7, IL-8, IL-3, and chemokine), Wnt/β-catenin, androgen, PTEN, p53, TGF-β, and circadian clock regulation. A total of 168 concordantly methylated genes were identified, with 109 genes (65%) showing increased methylation in AA CAFs and TAS (p-value < 0.05). Treatment with 5-AzaC significantly reduced DNA methylation of concordant genes in AA CAFs (p-value < 0.001). Conclusions: These findings suggest a distinct stromal methylome in AA, providing a foundation for integrating demethylating agents into standard therapies. This approach targets the tumor microenvironment, potentially addressing PCa disparities in AA men. Full article

Basal cell carcinoma (BCC), the most common skin cancer, is primarily driven by Hedgehog (Hh) and TP53 pathway alterations. Although additional pathways were implicated, the mutational landscape in Asian populations, particularly Koreans, remains underexplored. We performed whole-exome sequencing of BCC tumor tissues from Korean patients and analyzed mutations in 11 established BCC driver genes (PTCH1, SMO, GLI1, TP53, CSMD1/2, NOTCH1/2, ITIH2, DPP10, and STEAP4). Mutational profiles were compared with Caucasian cohort profiles to identify ethnicity-specific variants. Ultraviolet (UV)-exposed and non-UV-exposed tumor sites were compared; genes unique to non-UV-exposed tumors were further analyzed with protein–protein interaction analysis. BCCs in Koreans exhibited distinct features, including fewer truncating and more intronic variants compared to Caucasians. Korean-specific mutations in SMO, PTCH1, TP53, and NOTCH2 overlapped with oncogenic gain-of-function/loss-of-function (GOF/LOF) variants annotated in OncoKB, with some occurring at hotspot sites. BCCs in non-exposed areas showed recurrent mutations in CSMD1, PTCH1, and NOTCH1, suggesting a UV-independent mechanism. Novel mutations in TAS1R2 and ADCY10 were exclusive to non-exposed BCCs, with protein–protein interaction analysis linking them to TP53 and NOTCH2. We found unique ethnic-specific and UV-independent mutational profiles of BCCs in Koreans. TAS1R2 and ADCY10 may contribute to tumorigenesis of BCC in non-exposed areas, supporting the need for population-specific precision oncology. Full article

Plant callus cultures are a sustainable alternative for producing bioactive secondary metabolites, but their low yields limit industrial applications. Carob (Ceratonia siliqua L.) is rich in medicinally valuable compounds, yet conventional cultivation faces challenges. To address this, we use biofortified calcium phosphate nanoparticles, which refer to CaP-NPs that have been enriched with bioactive compounds via green synthesis using Jania rubens extract, thereby enhancing their functional properties as elicitors in carob callus. CaP-NPs were green-synthesized using Jania rubens extract and applied to 7-week-old callus cultures at 0, 25, 50, and 75 mg/L concentrations. At the optimal concentration (50 mg/L), CaP-NPs increased callus fresh weight by 23.9% and dry weight by 35.1%. At 50 mg/L CaP-NPs, phenolic content increased by 95.7%, flavonoids by 34.4%, tannins by 131.8%, and terpenoids by 211.9% compared to controls. Total antioxidant capacity rose by 76.2%, while oxidative stress markers malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) decreased by 34.8% and 14.1%, respectively. Gene expression analysis revealed upregulation of PAL (4-fold), CHI (3.15-fold), FLS (1.16-fold), MVK (8.3-fold), and TA (3.24-fold) at 50 mg/L CaP-NPs. Higher doses (75 mg/L) induced oxidative damage, demonstrating a hormetic threshold. These findings indicate that CaP-NPs effectively enhance secondary metabolite production in carob callus by modulating biosynthetic pathways and redox balance, offering a scalable, eco-friendly approach for pharmaceutical and nutraceutical applications. Full article

Diabetic nephropathy (DN) represents a severe microvascular complication of diabetes mellitus. As a Traditional Chinese Medicine (TCM) with extensive clinical applications, Ligustri Lucidi Fructus (LLF) exhibits significant anti-DN activity. However, the underlying pharmacological mechanisms, crucial components, and targets for LLF in DN treatment remain unclear. By integrating network pharmacology, molecular docking, and molecular dynamics simulations, the bioactive compounds, potential therapeutic targets, and underlying mechanisms of LLF in the treatment of DN were elucidated, followed by biological validation in a palmitic acid (PA)-induced MPC5 podocyte injury model. Among the 383 DN-related LLF targets identified, TNF emerged as a pivotal one, demonstrating potential binding interaction with the active components salidroside (Sal), apigenin (Api), and tormentic acid (TA). Moreover, Gene Expression Omnibus (GEO) database and KEGG enrichment analysis collectively highlighted the cytosolic DNA-sensing pathway. Notably, the cGAS-STING pathway is central to this pathway. Experimental studies further demonstrated that LLF-containing serum exerted a protective effect on MPC5 podocytes through cGAS-STING pathway suppression. Overall, these findings elucidate the pleiotropic mechanisms underlying LLF’s protective effects against DN, integrating compound–target–pathway interactions and thus offering a rationale for further investigation. Full article

Background/Objectives: Vancomycin-induced nephrotoxicity (VIN) remains a significant clinical challenge, with no effective nephroprotective agent currently established. This study aimed to evaluate the protective effects of the sodium–glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin (DAPA) against VIN in a Wistar albino rat model. Methods: Rats were randomly assigned to four groups: control, VA (vancomycin), DAPA (dapagliflozin), and VA+DAPA. Renal function was assessed by measuring serum urea and creatinine. Oxidative stress markers [malondialdehyde (MDA), total oxidant status (TOS), and myeloperoxidase (MPO)], antioxidant enzyme activities [total antioxidant status (TAS), glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD)], apoptotic mediators (Bax, Bcl-2, and caspase-3), and pro-inflammatory cytokines [tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6)] were evaluated. Histopathological and immunohistochemical analyses of kidney tissues were also performed. Results: Administration of VA led to significant renal dysfunction, increased oxidative stress, heightened apoptotic activity, and notable histopathological damage. Co-administration of DAPA with VA significantly reduced serum urea and creatinine levels and decreased caspase-3 activity and was associated with a trend toward reduction in both MDA levels and TNF-α expression, as well as the amelioration of histopathological renal injury. However, reductions in IL-1β and IL-6 levels were not statistically significant. Overall, these findings indicate that DAPA exerts nephroprotective effects against VIN by modulating oxidative stress, inflammation, and apoptotic pathways. Conclusions: Dapagliflozin may serve as a potential protective agent against vancomycin-induced nephrotoxicity. Further long-term and large-scale clinical studies are warranted to validate these preclinical findings and explore their therapeutic implications. Full article

Humans are continuously exposed to blue light from sunlight, computers, and smartphones. While blue light has been reported to affect living organisms, its role in fat synthesis and weight changes remains unclear. In this study, we investigated the effects of prolonged blue light exposure on weight changes in mice and the protective role of tranexamic acid (TA). Mice were exposed daily to blue light from a light-emitting diode for five months. Blue light exposure led to increased fat mass and body weight. The expression of the clock genes arnt-like 1 (Bmal1) and Clock was reduced in the brain and muscle of exposed mice. In addition, reduced Sirt1 and increased mammalian target of rapamycin complex 1 (mTORC1)/sterol regulatory element-binding protein 1 (SREBP1) were observed. The levels of liver X receptor a and liver kinase B1/5′AMP-activated protein kinase a1, both involved in SREBP1-mediated lipogenesis, were also elevated. TA treatment prevented the blue light-induced suppression of Bmal1/Clock and modulated the subsequent series of signal transduction. These findings suggest that prolonged blue light exposure suppresses the clock gene Bmal1/Clock, reduces Sirt1, and activates lipogenic pathways, contributing to weight gain. TA appears to regulate clock gene expression and mitigate blue light-induced weight gain. Full article

Background/Objectives: Sweet taste receptor TAS1R2 is expressed in skeletal muscle, yet its role in muscle metabolism remains poorly understood. Methods: Here, we leverage the BXD recombinant inbred mouse panel and Tas1r2 whole-body knockout (bKO) models to investigate the transcriptional impact of Tas1r2 deficiency on skeletal muscle function. Results: A gene network analysis revealed significant overlap in transcriptomic signatures between BXD strains with low Tas1r2 expression (BXD L_Tas1r2) and bKO muscle, particularly in pathways regulating oxidative phosphorylation, cytoplasmic ribosome function, and proteostasis. Notably, Tas1r2 expression negatively correlated with genes involved in fatty acid metabolism, suggesting its role in lipid utilization. Under high-fat diet (HFD) conditions, BXD_HFD L_Tas1r2 mice exhibited further enrichment in pathways linked to proteasome degradation, oxidative stress, and interleukin signaling, amplifying the transcriptomic convergence with bKO models. Key transcription factors (Mlxipl, Nfic, Rxrb) exhibited altered regulatory patterns under dietary stress, indicating that TAS1R2 influences metabolic adaptability through transcriptional reprogramming. Conclusions: Given that human TAS1R2 variants rarely result in complete loss of function (LOF), the BXD panel provides an effective dose-dependent model to bridge the gap between knockout phenotypes and human SNP carriers. Our findings establish TAS1R2 as a metabolic regulator in skeletal muscle and highlight the utility of genetically diverse mouse populations in dissecting gene-diet interactions relevant to human metabolic diseases. Full article

Solar-driven interfacial evaporation has emerged as a sustainable and highly efficient technology for seawater desalination, attracting considerable attention for its potential to address global water scarcity. However, challenges such as low evaporation rates and salt accumulation significantly hinder the performance and operational lifespan of evaporators. Here, we present an innovative Janus-structured evaporator featuring distinct operational mechanisms through the integration of a hydrophobic PVDF-HFP@PPy photothermal membrane and a hydrophilic PVA-CF@TA-Fe³⁺ hydrogel, coupled with a unidirectional flow configuration. Distinct from conventional Janus evaporators that depend on interfacial water transport through asymmetric layers, our design achieves two pivotal innovations: (1) the integration of a lateral fluid flow path with the Janus architecture to enable sustained brine replenishment and salt rejection and (2) the creation of dual vapor escape pathways (hydrophobic and hydrophilic layers) synergized with hydrogel-mediated water activation to elevate evaporation kinetics. Under 1 sun illumination, the evaporator achieves a maximum evaporation rate of 2.26 kg m⁻² h⁻¹ with a photothermal efficiency of 84.6%, in both unidirectional flow and suspension modes. Notably, the evaporation performance remains stable across a range of saline conditions, demonstrating remarkable resistance to salt accumulation. Even during continuous evaporation of highly saline water (10% brine), the evaporator maintains an evaporation rate of 2.10 kg m⁻² h⁻¹ without observable salt precipitation. The dual anti-salt strategies—enabled by the Janus structure and unidirectional flow design—underscore the evaporator’s capability for sustained high performance and long-term stability in saline environments. These findings provide valuable insights into the development of next-generation solar evaporators that deliver high performance, long-term stability, and robustness in saline and hypersaline environments. Full article

A comparative transcriptomic analysis was conducted for the nitrogen-efficient (BNI-Munal) and derivative parent Munal wheat genotypes to unravel the gene expression patterns across four nitrogen levels (0%, 50%, 75%, and 100%). Analyzing the genes of BNI-enabled wheat helps us understand how they are expressed differently, which heavily influences BNI activity. Grain yield and 1000-grain weight were higher in BNI Munal than in Munal. All the other traits were similar in performance. Varying nitrogen dosages led to significant differences in gene expression patterns between the two genotypes. Genes related to binding and catalytic activity were prevalent among molecular functions, while genes corresponding to cellular anatomical entities dominated the cellular component category. Differential expression was observed in 371 genes at 0%N, 261 genes at 50%N, 303 genes at 75%N, and 736 genes at 100%N. Five unigenes (three upregulated and two downregulated) were consistently expressed across all nitrogen levels. Further analysis of upregulated unigenes identified links to the NrpA gene (involved in nitrogen regulation), tetratricopeptide repeat-containing protein (PPR), and cytokinin dehydrogenase 2. Analysis of downregulated genes pointed to associations with the Triticum aestivum 3BS-specific BAC library, which encodes the NPF (Nitrate and Peptide Transporter Family) and the TaVRN gene family (closely related to the TaNUE1 gene). The five unigenes and one unigene highlighted in the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were validated in Munal and BNI Munal. The results obtained will enhance our understanding about gene expression patterns across different nitrogen levels in BNI wheat and help us breed wheat varieties with the BNI trait for improved NUE. Full article

Cadmium (Cd) contamination in agricultural soils poses a significant threat to human health through the food chain. It is of great significance to address safe wheat production in Cd-contaminated agricultural soils. This study employed foliar spraying of ferulic acid (FA) in both hydroponic and field trials to investigate its potential in alleviating Cd toxicity and reducing Cd accumulation in wheat grains. Our findings revealed that FA application at 20 and 50 μM promoted plant growth, increased photosynthetic efficiency, and enhanced root tolerance to Cd by increasing mean root diameter, surface area, and root tip number, as well as enhancing antioxidant defense in roots. Especially, 20 μM FA foliar application significantly alleviated Cd-induced growth inhibition in seedlings and reduced grain Cd content by 66.3% compared to Cd-stressed alone. Mechanistically, FA downregulated the Cd transporter gene TaHAM2 to reduce Cd translocation from roots to shoots, while upregulated the Cd cellular compartment gene TaHAM3 to increase root Cd retention, of which 82.9% was sequestered in roots. During the grain-filling period in the field trial, FA application reduced Cd transport from roots to stems and stems to rachides, but enhanced Cd retention in rachides and roots. Additionally, FA downregulated the phloem Cd loading gene LCT1, limiting Cd allocation to bracts and grains, which in turn lowered the Cd content in the grains. Collectively, FA foliar application modulated Cd transport pathways by coordinately downregulating xylem and phloem transporter genes and enhancing root Cd retention capacity. These findings established FA as a promising strategy for Cd detoxification and reduced accumulation in crop grains through integrated physiological and molecular interventions. Overall, it holds potential for the future development of safe crop production in soils polluted with Cd. Full article

Wheat (Triticum aestivum) is one of the most important cereal crops globally, with significant economic value. The Arabidopsis Tóxicos en Levadura (ATL) gene family, which comprises members of ubiquitin ligase enzymes (E3s), functions in substrate protein tagging during ubiquitin-mediated protein modification. Recent studies have demonstrated its involvement in stress responses. However, the ATL gene family in wheat remains poorly characterized. This study aimed to identify the members of the ATL gene family in wheat and investigate their roles under salt stress. We identified 334 TaATL genes in the wheat genome, all of which contain either RING-H2, RING U-box, or RAD18 superfamily domains, exhibiting a remarkably low proportion of intron-containing genes. The Ka/Ks (non-synonymous to synonymous substitution rate) analysis and cis-acting element analysis of the TaATL gene family indicate that its sequences are highly conserved and functionally constrained, suggesting that it may participate in abiotic stress responses through the ABA, MeJA, and MYB signaling pathways. Both RNA-seq analysis and RT-qPCR data demonstrated that the expression levels of the TaATL gene family were significantly upregulated under stress conditions, indicating their crucial roles in stress responses. This study demonstrates that the targeted regulation of stress-responsive signaling pathways mediated by superior TaATL gene family members can effectively enhance wheat salt tolerance, thereby providing a viable strategy for the development of high-yielding cultivars adapted to saline agricultural ecosystems. Full article