Cucumber is a core cultivated facility vegetable in China. Drought stress at the seedling stage severely inhibits its growth and development. The regulatory mechanism and optimal application concentration of SiO2 nanoparticles in alleviating drought stress in cucumber seedlings remain unclear. Moreover, traditional manual measurement and classic point cloud segmentation models struggle to achieve high-throughput accurate detection of cucumber seedling phenotypes under drought stress. To address these issues, this study focused on phenotypic detection under drought stress and analysis of the regulatory effects of SiO2 nanoparticles. An improved compact and low-redundancy segmentation model, DDCANet, was proposed based on PointNet++-SSG. Combined with 3D point cloud technology and the Euclidean clustering algorithm, it enables automatic extraction of phenotypic parameters from cucumber seedlings treated with SiO2 nanoparticles under drought stress. In this study, Trailing cucumber seedlings were used as experimental materials. 3D point cloud data of cucumber seedlings were collected under treatments with different concentrations of SiO2 nanoparticles and PEG-simulated drought stress. A dataset containing 70 valid samples was constructed and labeled into two categories: Stem and Leaf. The core optimizations of the DDCANet model are as follows: Firstly, an Adaptive Density-Aware Feature Enhancement (ADFE) module is embedded to accurately capture point cloud density heterogeneity induced by SiO2;Secondly, a Channel Attention and Normalization-enhanced SA Layer (CANL) is designed to strengthen the coupling of local and global drought-related phenotypic features. Thirdly, a Drought-Aware Hybrid Loss (DHL) function is constructed to alleviate the class imbalance of seedling stem and leaf point clouds under drought stress. Results show that the DDCANet model achieves a mean Intersection over Union (mIoU) of 89.01 ± 0.32% and a Stem IoU of 83.6 ± 0.45%, representing improvements of 6.55% and 9.6% respectively compared with the baseline PointNet++-SSG model, and a 30.5% improvement in stem segmentation accuracy compared with the classic PointNet model. It thus enables high-throughput, non-destructive detection of drought phenotypes in cucumber seedlings under SiO2 nanoparticle treatment. Ablation experiments verified the positive contributions of the ADFE, CANL, and DHL modules. Furthermore, instance segmentation and phenotype extraction were completed using the Euclidean clustering algorithm to analyze the drought-alleviating effects of SiO2 nanoparticles under PEG-simulated drought stress. Results indicate that a low concentration of 20 mg/L exhibits a weak alleviating effect, medium concentrations of 40-60 mg/L show bidirectional regulatory characteristics, and a high concentration of 100 mg/L causes negative physiological effects. The optimal application concentration is 80 mg/L, which comprehensively improves key phenotypes such as seedling height and volume under drought stress and exerts a positive regulatory effect on seedling growth under drought conditions. The DDCANet model constructed in this study provides an efficient technical tool for the accurate phenotypic detection of crop seedlings treated with SiO2 nanoparticles under drought stress. It clarifies the optimal application concentration of SiO2 nanoparticles, offers a precise concentration threshold and theoretical support for the scientific application of SiO2 nanoparticles in drought-stressed cultivation of protected cucumber, and establishes a novel methodological reference for the research on phenotypic regulation of crops under drought stress via nano-agricultural technology.

Neurodegenerative diseases (NDs), such as Alzheimer's disease, Parkinson's disease, and Huntington's disease are discussed as representative examples of conditions in which oxidative stress and proteostasis imbalance contribute to progressive neuronal dysfunction. Oxidative stress, defined as an imbalance between reactive oxygen species (ROS) production and antioxidant defenses, is widely recognized as a key contributor to ND pathogenesis. Excessive ROS disrupt cellular homeostasis and promotes protein misfolding and aggregation, thereby compromising the proteostasis network. In response to this stress, molecular chaperones, including members of heat shock protein (Hsp) family, play a crucial protective role by maintaining protein folding integrity and preventing toxic aggregation. Furthermore, mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) serve as carriers of bioactive molecules, including antioxidants and molecular chaperones, offering a unique mechanism to restore cellular homeostasis. This review explores the interplay between oxidative stress and molecular chaperones in the pathogenesis of NDs and highlights the emerging therapeutic potential of MSC-EVs as modulators of oxidative and proteostatic imbalance.

Diabetes mellitus is a multifactorial metabolic disorder driven by dysregulated signaling networks, and its complications are closely associated with insulin resistance, metabolic imbalance, oxidative stress, chronic inflammation, mitochondrial dysfunction, and disturbed cell-fate control. Astragaloside IV (AS-IV), a major bioactive saponin derived from Astragalus membranaceus, has attracted increasing attention as a multi-target candidate for diabetes and diabetes-related complications. This review summarizes recent advances in the signaling pathway-mediated anti-diabetic mechanisms of AS-IV, with particular emphasis on the integrated regulation of PI3K/Akt, AMPK, NF-κB, Nrf2/HO-1, mTOR, MAPK, and cell-fate-related pathways. Current evidence indicates that AS-IV improves insulin sensitivity and glucose metabolism through PI3K/Akt activation, regulates energy and lipid metabolism via AMPK-related signaling, suppresses inflammatory amplification by inhibiting NF-κB and NLRP3 inflammasome activation, and alleviates oxidative injury through activation of the Nrf2/HO-1 antioxidant axis. In addition, AS-IV modulates autophagy, apoptosis, ferroptosis, and mitochondrial homeostasis, thereby contributing to organ protection in diabetic kidney disease, cardiovascular complications, retinopathy, neuropathy, and diabetic foot ulcers. Compared with previous reports that mainly focused on isolated pathways or single complications, this review highlights a network-level and multi-pathway integration perspective, emphasizing the cross-talk among metabolic regulation, inflammation, oxidative stress, mitochondrial function, and programmed cell fate. Nevertheless, most current evidence remains derived from preclinical models, and important translational barriers, including low bioavailability, heterogeneous dosing regimens, insufficient pharmacokinetic-pharmacodynamic data, and limited clinical validation, still need to be addressed. Future studies integrating standardized disease models, multi-omics strategies, clinical samples, and well-designed prospective trials are required to clarify the therapeutic positioning of AS-IV and facilitate its translation as a potential multi-target agent for diabetes therapy.

Inflammatory bowel disease (IBD), primarily comprising Crohn's disease and ulcerative colitis, represents a group of chronic, relapsing intestinal inflammatory conditions mediated by immune dysregulation. Emerging evidence has established the gut microbiota and its metabolic products as central players in IBD pathogenesis. The human gut microbiota constitutes a vast and dynamic micro-ecosystem whose metabolic activities generate a diverse array of small molecules, including short-chain fatty acids, bile acids, and tryptophan-derived metabolites. These metabolites collectively form a "gut microbiota-metabolite-immune axis" that is deeply involved in maintaining intestinal homeostasis, and their dysregulation is closely linked to IBD initiation and progression. Patients with IBD typically exhibit significant alterations in gut microbial composition and function, with key metabolic perturbations characterized by reduced levels of SCFAs and secondary bile acids, as well as imbalances in specific amino acid-derived metabolites. SCFAs not only serve as essential energy substrates for colonic epithelial cells but also modulate immune responses and enhance barrier integrity through G protein-coupled receptors and inhibition of histone deacetylases. Bile acids contribute to barrier function and immune balance via activation of nuclear receptors such as the farnesoid X receptor and the G protein-coupled bile acid receptor 1. Tryptophan, metabolized by both host enzymes and the gut microbiota into kynurenine, serotonin, and various indole derivatives, participates in immunoregulation through pathways involving the aryl hydrocarbon receptor. These examples underscore the pivotal roles of gut microbial metabolites in both the pathogenesis and treatment of IBD. This review aims to synthesize recent advances in understanding the functions and molecular mechanisms of key gut microbial metabolites in IBD, with a focus on how they orchestrate the initiation and perpetuation of intestinal inflammation through complex immunoregulatory networks and modulate intestinal barrier function. By providing new insights into the mechanisms underlying IBD pathogenesis and intervention, this review seeks to establish a theoretical foundation for the development of novel diagnostic and therapeutic strategies targeting microbial metabolites.

Patients with diabetes exhibit increased susceptibility to myocardial ischemia/reperfusion (IR) injury. Emerging evidence highlights gut microbiota-derived microbial metabolites as critical modulators of the gut-heart axis. This study examined the pathological role of succinate, a crucial metabolite derived from the microbiota, in the progression of diabetic myocardial IR injury.

Protein-RNA phase separation gives rise to biomolecular condensates with rich internal organization, yet the molecular rules that connect sequence-encoded interactions to the emergent condensate spatial organization remain poorly understood. Here, using large-scale residue-level coarse-grained simulations, we identify a molecular grammar that governs the formation of multiphase protein-RNA condensates. We show that asymmetries in protein-protein and protein-RNA interactions, together with protein stoichiometry, chain length, and condensate density, collectively determine whether condensates adopt homogeneous, layered, biphasic, or vesicle-like morphologies. Vesicular condensates form spontaneously from well-mixed initial conditions without requiring flux-driven oversaturation or extreme charge imbalance, distinguishing this mechanism from previously proposed routes to condensate hollowing. We rationalize the full morphological progression as sequence-encoded amphiphile self-assembly: the protein-RNA complex behaves as a single-chain amphiphile whose effective packing parameter is set by Domain H/L stoichiometry, spanning micelles, cylinders, hollow vesicles, and inverse phases.

Alzheimer's disease (AD) involves not only amyloid-β and tau pathology but synaptic dysfunction and impaired autophagy, though the underlying mechanisms and their relationship to AD progression are not well understood. Transsynaptic complexes involving presynaptic neurexins (Nrxn1/2/3), secreted cerebellins (Cbln1/2/3/4), and postsynaptic glutamate delta receptors (GluD1/2) play critical roles in organizing synapses and synaptic plasticity. Studies in pain models have reported that treatment with recombinant Cbln1 rescues AMPA glutamate receptor imbalance, promotes autophagy, and inhibits hyperexcitability and pain behaviors. Here we tested the novel hypothesis that dysregulation of Cbln-GluD-based transsynaptic complexes may occur in the brain of AD patients, providing insights into disease progression and potential avenues for therapeutic development.

Boron (B) is an essential micronutrient, yet its excess induces phytotoxicity, especially in semi-arid and alkaline soils, severely constraining crop productivity. This review delineates the physiological, biochemical, and molecular responses of plants to B toxicity, highlighting oxidative stress, membrane disruption, metabolic imbalance, and photosynthetic impairment as primary consequences. Multi-omics studies, including transcriptomics, proteomics, and metabolomics, have identified key components of B tolerance, such as BOR and NIP transporters, antioxidant enzymes, and stress-inducible proteins. Proteomic investigations reveal tissue-specific responses, with the upregulation of detoxification proteins, SA-dependent defence proteins, and transcriptional regulators like RING1B, which is also implicated in stem cell maintenance. Emerging evidence underscores the role of epigenetic modifications, DNA methylation, and histone acetylation in modulating B-responsive gene expression. However, the absence of high-resolution spatial mapping of B toxicity zones and limited access to high-throughput phenotyping platforms hinder progress in breeding resilient genotypes. Additionally, the interplay between B toxicity and climate change remains underexplored, despite its likely influence on B solubility and plant uptake. Advancements in nanotechnology and microbiome engineering present novel strategies for mitigation, including nano-sensors for real-time B detection, nano-formulations for controlled delivery, and beneficial microbes for enhancing plant tolerance. Integrating these tools with precision breeding and systems biology offers a sustainable framework to counteract B toxicity. This review advocates for a transdisciplinary approach combining spatial analytics, molecular insights, and ecological resilience to manage B toxicity and ensure long-term agricultural sustainability.

Tropospheric ozone (O3) pollution and potentially toxic elements (PTEs) contamination are two of the most inescapable abiotic stressors threatening plant productivity and ecosystem stability. Independently, these stressors induce profound physiological and biochemical disruptions in plants, including oxidative stress, impaired stomatal function, and nutrient imbalances. Ozone primarily affects the apoplast, triggering reactive oxygen species (ROS)-mediated signalling, stomatal closure, and reprogramming of defense-related gene expression. While PTEs infiltrate cellular compartments, compromising photosynthesis, enzyme activities, and redox balance. Emerging studies reveal that their co-occurrence can produce antagonistic, synergistic, or additive possessions, depending on plant species, developmental stage, exposure intensity and experimental system. Both the stressors unite on oxidative stress (ROS) and antioxidant responses, stomatal behaviour, photosynthetic apparatus damage and altered nutrient and metal uptake/partitioning. However, insights into their combined impacts remain scarce. Literature is fragmented by methodological heterogeneity, limited crop coverage, and a lack of comprehensive omics, tracer and transport studies. This review scrutinizes the mechanistic responses of plants to individual and concurrent exposures to O₃ and PTEs, focusing on antioxidant defense systems, signaling networks, and key physiological traits. Additionally, we explore transcriptomic shifts that command acclimation or vulnerability, highlighting the molecular pathways that administrate plant responses under these stress conditions. Understanding these interactions is crucial for breeding resilient crop varieties and optimizing phytoremediation stratagems in polluted agroecosystems. Finally, this synthesis emphasizes the urgent need for multifactorial studies, standardized protocols, and validation under diverse soil and climatic conditions, crop genotypes and O₃ regimes to more accurately predict plant behaviour under real-world environmental stress scenarios.

Radiotherapy has emerged as a cornerstone modality in the management of malignant tumors. Its evolution from a localized intervention to a radical curative strategy has been particularly pronounced in lung cancer, where its role has shifted from symptom palliation to survival prolongation. Radiation esophagitis (RE) is one of the most common acute adverse effects of thoracic radiotherapy, particularly in patients with lung cancer. In the early phase of RE, the predominant features include reactive oxygen species-mediated DNA damage and disruption of the epithelial barrier. The inflammatory phase is characterized by nuclear factor kappa B activation, edema, and pain. During the dysregulated repair phase, impaired regeneration of the esophageal mucosal epithelium, compounded by microbiota imbalance, further exacerbates tissue injury. In the late phase, transforming growth factor beta-driven fibrosis may culminate in stricture or fistula formation. Clinically, the condition primarily manifests as dysphagia and odynophagia. The prevention and management of RE remain significant clinical challenges. This review examines key issues related to RE within the context of precision radiotherapy, with particular emphasis on its incidence and current management strategies.