Superoxide dismutase (SOD) serves as a critical regulator of plant stress adaptation to salinity, drought, and heavy metal toxicity. Flax (Linum usitatissimum L.), a globally cultivated oilseed and fiber crop, lacks comprehensive genomic characterization of its SOD gene family. Here, we systematically identified 12 LuSOD genes in the flax genome. Phylogenetic reconstruction of SOD homologs across diverse plant species classified these genes into three evolutionarily conserved subgroups: Cu/Zn-SOD (6 LuCSD), Fe-SOD (3 LuFSD), and Mn-SOD (3 LuMSD). Comparative analysis of exon-intron architectures and conserved motifs revealed high structural conservation among LuSOD members within each clade. Promoter cis-element profiling identified predominant associations with phytohormone signaling (abscisic acid, methyl jasmonate) and abiotic stress responses, including hypoxia, drought, and low-temperature adaptation. MicroRNA target prediction identified lus-miR159 as the primary regulatory miRNA interacting with LuSOD genes. Gene ontology (GO) enrichment highlighted LuSOD roles in stress perception, metal ion chelation, and enzymatic reactive oxygen species (ROS) scavenging. Transcriptomic profiling demonstrated ubiquitous high expression of LuSOD genes in leaf tissues. qRT-PCR validation under cold, drought, and salt stresses revealed significant upregulation of nine LuSOD genes, implicating their involvement in antioxidant defense mechanisms. Functional characterization of LuCSD3 in transgenic Arabidopsis confirmed its role in enhancing salt tolerance through ROS homeostasis modulation. This study provides foundational insights into LuSOD-mediated stress resilience, serving as a valuable resource for molecular breeding and functional genomics in flax.

Background/Objectives: Blunt cardiac injury (BCI) is a severe medical condition that may arise as a result of various traumas, including motor vehicle accidents and falls. The main objective of this study was to explore the role and underlying mechanisms of the TRPV4 gene in BCI. Elucidating the function of TRPV4 in BCI may reveal potential novel therapeutic targets for the treatment of this condition. Methods: Rats in each group, including the SD control group (SDCON), the SD blunt-trauma group (SDBT), the TRPV4 gene-knockout control group (KOCON), and the TRPV4 gene-knockout blunt-trauma group (KOBT), were all freely dropped from a fixed height with a weight of 200 g and struck in the left chest with a certain energy, causing BCI. After the experiment, the levels of serum IL-6 and IL-1β were detected to evaluate the inflammatory response. The myocardial tissue structure was observed by HE staining. In addition, cardiac transcriptome analysis was conducted to identify differentially expressed genes, and metabolomics studies were carried out using UHPLC-Q-TOF/MS technology to analyze metabolites. The results of transcriptomics and metabolomics were verified by qRT-PCR and Western blot analysis. Results: Compared with the SDCON group, the levels of serum IL-6 and IL-1β in the SDBT group were significantly increased (p < 0.001), while the levels of serum IL-6 and IL-1β in the KOBT group were significantly decreased (p < 0.001), indicating that the deletion of the TRPV4 gene alleviated the inflammation induced by BCI. HE staining showed that myocardial tissue injury was severe in the SDBT group, while myocardial tissue structure abnormalities were mild in the KOBT group. Transcriptome analysis revealed that there were 1045 upregulated genes and 643 downregulated genes in the KOBT group. These genes were enriched in pathways related to inflammation, apoptosis, and tissue repair, such as p53, apoptosis, AMPK, PPAR, and other signaling pathways. Metabolomics studies have found that TRPV4 regulates nucleotide metabolism, amino-acid metabolism, biotin metabolism, arginine and proline metabolism, pentose phosphate pathway, fructose and mannose metabolism, etc., in myocardial tissue. The combined analysis of metabolic and transcriptional data reveals that tryptophan metabolism and the protein digestion and absorption pathway may be the key mechanisms. The qRT-PCR results corroborated the expression of key genes identified in the transcriptome sequencing, while Western blot analysis validated the protein expression levels of pivotal regulators within the p53 and AMPK signaling pathways. Conclusions: Overall, the deletion of the TRPV4 gene effectively alleviates cardiac injury by reducing inflammation and tissue damage. These findings suggest that TRPV4 may become a new therapeutic target for BCI, providing new insights for future therapeutic strategies.

Monoclonal antibodies are emerging as advanced therapies in companion-animal medicine, with approved or clinically evaluated applications in canine and feline osteoarthritis pain, canine atopic dermatitis, and selected infectious-disease and oncological settings. This critical narrative review integrates peer-reviewed studies, regulatory records, product information, and publicly available therapeutic-antibody sequence resources to examine target biology, species adaptation, Fc function, developability, and clinical implementation. Anti-NGF and anti-IL-31 products demonstrate the clinical value of long dosing intervals, whereas oncology and infectious-disease programmes remain subject to indication-specific efficacy and safety requirements. Canine and feline IgG subclasses, Fc-receptor and FcRn biology, incomplete feline framework resources, manufacturing economics, and owner-funded care all influence candidate design and deployment. Emerging bispecific antibodies, antibody–drug conjugates, VHHs, mRNA-based approaches, and AI-assisted strategies are most relevant when they address a defined veterinary use case. We propose a translational framework linking target validation, species-adapted engineering, species-matched assays, manufacturability, regulatory evidence, and real-world deployment.

Rabbit monoclonal antibodies (RabMAbs) are valuable for biomedical research and diagnostic applications because of their high affinity, specificity, and broad epitope recognition; here, we established an integrated phenotype-linked workflow for rapid RabMAb discovery using serum-derived polyclonal mouse IgG as a proof-of-concept model antigen. Three Big-Eared White rabbits were immunized in parallel, and the rabbit exhibiting the highest serum endpoint titer was selected for the complete downstream single-B-cell discovery workflow. Approximately 5 × 10⁵ activated B cells were subjected to polydisperse oblate dispersion system (POD)-based screening, yielding 13,266 antigen-positive POD events. Following recovery and 10× Genomics single-cell V(D)J sequencing, 4294 B-cell barcodes yielded valid/interpretable V(D)J data, of which 2099 contained at least one complete, productive, and translatable heavy-chain/light-chain pair, generating 2199 functional VH/VL pairing records. AbFinder™-assisted prioritization generated a computationally recommended pool of 158 candidates, and the five highest-ranked VH/VL pairs within this pool were selected for recombinant expression and validation. All five yielded antigen-reactive RabMAbs with an endpoint ELISA titer of 1:256,000 and BLI-derived apparent K_D values ranging from 4.19 × 10⁻¹⁰ to 9.79 × 10⁻⁹ M. The antibodies showed differential concentration-dependent reactivity toward mouse IgG1, IgG2a, IgG2b, and IgG3 preparations, weak reactivity toward human IgG, and clone-dependent reactivity toward rat IgG. The workflow from spleen collection to functional validation was completed within approximately three weeks. Because only five prioritized candidates from one selected responder rabbit were evaluated, the 5/5 validation outcome should not be interpreted as an overall platform hit rate or definitive validation of the prioritization algorithm. These findings support the feasibility of this workflow for research-grade and diagnostic antibody discovery, while broader evaluation will require larger candidate cohorts, independent biological validation, and additional antigen classes.

Renal fibrosis (RF) represents a major pathological outcome of chronic kidney disease, currently accompanied by extremely limited therapeutic strategies. To decipher key cellular and molecular drivers, we integrated single-cell and bulk transcriptomic profiles for comprehensive analysis. Based on the RF-related single-cell and bulk transcriptomic data, key cell subtypes were identified through Scissor analysis, custom signature matrix construction via CIBERSORTx, and Weighted Gene Co-Expression Network Analysis (WGCNA). Subsequently, key subtype-related biomarkers were identified through the expression analysis, and functional enrichment analysis for biomarkers was conducted to elucidate the potential mechanisms by which biomarkers regulate RF. Through comprehensive profiling, thick ascending limb (TAL) cells were predominant and displayed marked heterogeneity in renal fibrosis (RF), with cortical TAL (CTAL) and adaptive TAL (aTAL) identified as principal subtypes. A set of candidate biomarkers was identified. Quantitative polymerase chain reaction (qPCR) validation in mouse models confirmed aberrant expression of these biomarkers, with STAT1 and PARP8 upregulated and HS6ST2, PTGER3, and TMEM207 downregulated in RF. Furthermore, functional enrichment analyses indicated that these biomarkers were associated with pathways underlying metabolic reprogramming and immune perturbation. Our study implicates CTAL and aTAL as central cellular players in RF and identifies their associated biomarkers. These experimentally validated biomarkers provide novel targets and repurposing opportunities for RF therapeutic intervention.

Renal fibrosis represents the final common pathway of chronic kidney disease (CKD) progression and remains a major therapeutic challenge. Fibroblast growth factor receptor 3 (FGFR3) has emerged as a context-dependent component of fibroblast growth factor (FGF) signaling, but its renal role remains incompletely defined because direct receptor-specific evidence is scarce. This review integrates kidney-specific FGFR3 studies with endocrine FGF23–Klotho biology and broader FGF/FGFR networks using an explicit evidence hierarchy. Current direct renal evidence is limited to two 2025 experimental studies: an FGF18-associated FGFR3–AMPK–NOX4 program that attenuated folic acid-induced fibrosis, and a single toxicant model reporting an FGF9–FGFR3–PI3K/Akt program associated with fibroblast proliferation. The latter requires independent replication before generalization beyond toxicant nephropathy. By contrast, physiological renal FGF23 signaling is best established through FGFR1c–α-Klotho, whereas the strongest evidence for Klotho-independent pathological FGF23 signaling involves FGFR4 in cardiovascular tissues; direct evidence that FGF23 promotes renal fibrosis specifically through FGFR3 is lacking. Accordingly, FGFR3 should be viewed as an emerging, ligand- and compartment-dependent signaling component rather than a validated CKD therapeutic target. Future priorities include human kidney spatial and phosphoproteomic profiling, cell-specific FGFR3 perturbation, longitudinal FGF23/Klotho biomarker studies, and mechanism-based evaluation of FGFR-directed strategies with integrated renal and mineral-metabolism endpoints.