Search Results (7,649)

Fungal endophytes are symbiotic microorganisms that establish strong relationships inside plant tissues, providing potential advantages, especially in grasses, by enhancing tolerance to both abiotic and biotic stresses. This review investigates the molecular mechanisms through which fungal endophytes mediate stress tolerance, targeting host–pathogen interactions. By modulating pathogen-associated molecular patterns (PAMPs), damage-associated molecular patterns (DAMPs), and effector proteins, fungal endophytes may contribute to priming the plant’s immune system, enhancing its resistance to pathogen invasion. Moreover, endophyte colonization regulates core processes such as osmotic regulation, reactive oxygen species (ROS) detoxification, and secondary metabolite biosynthesis that enable plants to tolerate environmental stresses like drought, heat, and salinity. The review highlights the impact of endophytes on immune priming, systemic acquired resistance (SAR), and the regulation of non-coding RNAs that regulate host gene networks associated with stress tolerance. Furthermore, the integration of advanced multi-omics techniques genomics, transcriptomics, proteomics, metabolomics, and fluxomics has revealed emerging insights into the genetic and metabolic pathways driving these symbiotic associations. However, grass-specific molecular datasets remain limited, and the consistency of endophyte-mediated tolerance across host species and environmental conditions is not yet fully resolved. Fungal endophytes increase grass stress resilience through coordinated pathogen recognition, RNA regulation, and metabolic reprogramming while AI-assisted multi-omics approaches are emerging as tools for identifying candidate regulatory networks, although empirical validation in grass–endophyte systems remains limited. Together, these advances highlight the potential for climate-smart and sustainable crop improvement. Future research integrating functional genomics, field validation, and biosafety assessment will be essential for translating endophyte-based strategies into reliable agricultural applications. Full article

DNA methylation constitutes a primary layer of epigenetic regulation in plants, operating across three sequence contexts (CG, CHG, and CHH) through distinct enzymatic pathways. Over the past fifteen years, accumulating evidence has shown that DNA methylation varies substantially among individuals and populations of wild plants, sometimes independently of underlying genetic polymorphism. This variation can influence gene expression, transposable element activity, and phenotypic traits relevant to ecological adaptation. Population epigenetics, the study of methylation variation at the population scale, has matured from initial surveys using methylation-sensitive amplified fragment length polymorphism (MS-AFLP) into a discipline increasingly reliant on reduced-representation bisulfite sequencing (epiGBS, bsRADseq), whole-genome bisulfite sequencing (WGBS), enzymatic methyl-seq (EM-seq), and direct long-read detection by nanopore sequencing. These methodological advances are opening population epigenetics to non-model organisms across the full breadth of the plant phylogeny, from angiosperms and gymnosperms to ferns and bryophytes. We cover (i) the molecular machinery underlying plant DNA methylation, including the debated status of N6-methyladenine (6mA); (ii) empirical evidence for natural epigenetic variation in plant populations, spanning clonal, invasive, and outcrossing species; (iii) the methodological toolkit available for population-scale methylation profiling, with emphasis on approaches suitable for non-model taxa; and (iv) the ecological and evolutionary significance of population epigenetic variation, including transgenerational inheritance, stress memory, epigenetic clocks, conservation applications, and the emerging integration of epigenetics into the extended evolutionary synthesis. We identify critical knowledge gaps, particularly the near-complete absence of population-level epigenetic data for bryophytes, ferns, and lycophytes, and outline priorities for future research. Full article

Microplastic (MP) and nanoplastic (NP) pollution has emerged as a pervasive and still insufficiently quantified pressure on terrestrial ecosystems, yet its consequences for wild herbivores remain incompletely understood. As key links between primary producers and higher trophic levels, wild herbivores occupy a critical ecological position and may serve both as exposed receptors and as biological vectors of plastic contamination. This manuscript presents a narrative review that synthesizes recent advances in understanding the physiological, behavioural, and ecological implications of MP and/or NP exposure in free-ranging herbivorous mammals, integrating evidence from field surveys, experimental studies, ecological modelling, and supportive mechanistic findings from livestock and experimental mammalian systems. Available evidence indicates that MPs and NPs are consistently detected in wild herbivores from both human-modified and protected landscapes, demonstrating widespread terrestrial exposure. Reported biological effects include oxidative stress, digestive dysfunction, inflammatory and immune responses, altered gut microbial communities, impaired nutrient assimilation, and organ-level damage, although much of the mechanistic evidence derives from controlled laboratory or livestock-based studies rather than direct wildlife investigations. Behavioural responses remain comparatively underexplored, particularly in large-bodied herbivores, with limited evidence for altered foraging, habitat use, and stress-related behaviours. At the ecosystem level, emerging studies suggest that herbivores may contribute to the landscape-scale redistribution of MPs and NPs through movement and faecal deposition, with potential downstream effects on soil processes, nutrient cycling, and plant–herbivore interactions. However, the current evidence base is constrained by major methodological and conceptual limitations, including the lack of standardized detection and reporting protocols, limited ecological realism in exposure studies, taxonomic and geographic biases, and poor resolution of long-term population-level and food-web consequences. Overall, the available literature indicates that MP and NP pollution represent a multifaceted and emerging risk to wild herbivores and the ecosystems they inhabit. Future research should prioritize standardized contamination-controlled monitoring, non-invasive faecal surveillance, ecologically realistic chronic exposure studies, and integrated conservation frameworks that recognize wild herbivores as sentinel species for terrestrial plastic pollution. Full article

Mycotoxin contamination is an important threat to food and feed safety as well as human and animal health, with particular emphasis on oxidative stress, apoptosis, autophagy, inflammation, and dysbiosis. Mycotoxins represent major health threats because they disturb cellular homeostasis and induce oxidative damage. Nutritional factors, such as dietary antioxidants and bioactive chemicals, can influence the body’s reaction to mycotoxin exposure, either reducing or increasing its effects. This study discusses how mycotoxins (aflatoxin B1, deoxynivalenol, and ochratoxin A) induce oxidative stress by producing reactive oxygen species (ROS)-mediated DNA damage, which induces cellular damage and activates apoptosis, an intended cell death process that is critical for tissue integrity. Furthermore, mycotoxins alter autophagy, a cellular degradation process that can be beneficial or destructive depending on the situation, affecting cell survival. The inflammatory response is particularly important because mycotoxin-induced oxidative stress and cell damage activate inflammatory pathways, which contribute to tissue injury and disease progression. Nutritional factors high in antioxidants, anti-inflammatory substances (Lycopene, Curcumin, Thyme oil, Gum Arabic, and Ginger), probiotics, and prebiotics show potential in mitigating these negative consequences by reducing oxidative stress and inflammation. Advances in molecular biology and omics technologies (transcriptomics, proteomics, metabolomics, and single-cell sequencing) can lead to better knowledge of the underlying pathways, allowing for more tailored nutritional recommendations and medicinal interventions. Finally, combining dietary modulation with mycotoxin risk management is a viable path for protecting health and increasing resilience to mycotoxin-related toxicities in animals. Full article

Oxidative stress is a key contributor to the pathogenesis of immune-mediated diseases through its effects on cellular metabolism, mitochondrial function, immune signaling pathways, and inflammatory tissue injury. Disruption of redox homeostasis promotes metabolic reprogramming and persistent activation of innate and adaptive immune responses, contributing to disease progression across multiple inflammatory and autoimmune disorders. Recent advances in high throughput molecular technologies have generated large scale multi-omics datasets that enable comprehensive investigation of redox-associated mechanisms at a systems level. Integration of these datasets with computational analytical approaches has facilitated the identification of multidimensional molecular signatures associated with disease development and progression. This systematic review evaluates studies applying computational frameworks to analyze redox-related molecular data in immune-mediated diseases including multiple sclerosis, systemic lupus erythematosus, lupus nephritis, rheumatoid arthritis, Sjögren’s syndrome, and inflammatory bowel disease. Across the reviewed studies, oxidative stress associated with molecular signatures were consistently linked to immune activation, mitochondrial metabolism, and inflammatory signaling pathways. Computational analyses also identified regulatory genes involved in antioxidant defense and metabolic regulation, as well as pathways associated with regulated cell death. These findings highlight the translational potential of computational redox analysis for biomarker discovery, disease stratification, and development of targeted therapeutic strategies aimed at restoring redox balance and improving clinical management of immune-mediated diseases. Full article

Adult neural stem cells (NSCs) maintain lifelong neurogenesis, a fundamental process for neuroplasticity, memory and brain homeostasis. Despite decades of research, translating basic NSC biology into effective clinical therapies remains a central challenge. Here we present a narrative review that provides a comprehensive update on the current landscape of adult NSC research, associating molecular mechanisms with the emerging translational technologies. First, we analyze the biological features and neurogenic sequences within canonical niches such as the subventricular lateral zone and the subgranular zone, emphasizing phylogenetic and migratory differences between rodent models and humans. Second, we integrate these mechanisms with the influence of environmental and pathological modulators, describing how aging, metabolic changes, chronic stress and neuroinflammation disrupt NSC quiescence and lineage progression. Finally, we highlight recent technological advances driving the field toward clinical applications. By examining current NSC isolation strategies, induced pluripotent stem cell modeling, direct somatic reprogramming and the use of CRISPR-Cas9-based gene-editing therapies, this review delineates the pathways to overcome existing methodological limitations. Ultimately, we provide an integrated context that connects the modulation of the neurogenic niches with advanced in vitro technologies, offering new perspectives for regenerative medicine and the treatment of neurological disorders. Full article

Iodoacetic acid (IAA), a highly cytotoxic disinfection byproduct commonly detected in drinking water, poses a potential risk to female reproductive health. The direct molecular mechanisms underlying its effects on the reproductive system epithelium remain unclear. This study demonstrates that IAA induces glycational stress in primary porcine uterine (UECs) and oviduct epithelial cells (OECs), representing an early event contributing to extensive cellular toxicity. IAA exposure inhibited Glyceraldehyde-3-Phosphate Dehydrogenase (GAPDH) enzymatic activity and promoted the accumulation of advanced glycation end products (AGEs) Nε-(carboxymethyl)lysine (CML), triggering mitochondrial dysfunction, redox imbalance, calcium dyshomeostasis, and endoplasmic reticulum stress. These disturbances activated a dysregulated signaling network involving the p38 MAPK, AKT, and NF-κB pathways, ultimately causing G1/S cell cycle arrest and apoptosis. Notably, pretreatment with the AGE inhibitor pyridoxamine reduced CML accumulation, restored mitochondrial function, and alleviated apoptotic cell death. These findings identify glycational stress as a key initiating mechanism for IAA-induced reproductive epithelial toxicity, providing mechanistic insight into the potential health risks of environmental disinfection byproducts. Full article

Plants must constantly adapt to biotic and abiotic stressors, which the global climate change crisis has intensified. To monitor plant health and predict their ability to face these challenges, various target molecules, such as hormones, glucose, and reactive oxygen species, are used as proxies for their physiological status. This review provides a systematic assessment of the current state of biosensor technology, an innovative analytical approach designed for in situ, minimally invasive, and real-time monitoring. Using the PICO (Problem, Intervention, Comparison, and Outcome) strategy, relevant research papers were identified. The review highlights how biosensors can detect physiological responses to stress before visual symptoms manifest, offering a significant advantage over traditional, often destructive, laboratory techniques, like gas chromatography–mass spectrometer (GC-MS) or high-performance liquid chromatography (HPLC). These advancements aim to improve precision agriculture and forestry management by providing sustainable methods to assess resilience in changing environments. Finally, the challenges of translating research from model organisms to complex woody species and choosing the correct target are discussed, and future perspectives, including the integration of biosensors with Artificial Intelligence-driven predictive models for large-scale environmental monitoring, are outlined. Full article

Triplophysa yarkandensis (Cypriniformes: Nemacheilidae), a rare endemic fish in the Tarim River Basin, Xinjiang, China, plays a pivotal role in maintaining the stability of plateau saline–alkaline aquatic ecosystems, yet its survival is increasingly threatened by habitat salinization. However, the multi-dimensional synergistic adaptation mechanisms linking its phenotypic variation, intestinal structure, and associated microbial communities to extreme saline–alkaline stress remain poorly understood. In this study, we innovatively integrated morphological/intestinal histological characterization, 16S rRNA gene sequencing, and microbial ecological analyses (co-occurrence networks and assembly processes) to systematically decode its adaptive strategies. Results revealed that T. yarkandensis exhibits a streamlined body shape, morphological variability, and elongated intestinal villi that may support locomotion and nutrient/ion uptake under osmotic stress. Its gut exerts a stringent selective filter, driving distinct differentiation between water and gut microbial communities—with gut-enriched core taxa (Aurantimicrobium and Aestuariivirga) and functional pathways (unsaturated fatty acid biosynthesis and ABC transporters) specialized for osmoregulation. Notably, the water microbial assembly is dominated by stochastic processes, while the gut assembly relies on host-driven deterministic selection, forming a habitat-specific adaptive pattern. These findings uncover the synergistic adaptation system of host phenotype and gut microbiota for survival in extreme saline–alkaline habitats, advancing our understanding of fish–microbe co-evolution in extreme ecosystems and providing critical theoretical support for the conservation of rare plateau fish, as well as guidance for the utilization of saline–alkaline water resources in aquaculture. Full article

Oxidative stress is one of the few defined causes of male infertility affecting at least one third of patients attending infertility clinics. Human spermatozoa are vulnerable to this form of attack because their stripped-down architecture means that they possess limited antioxidant protection and little capacity for biochemical repair. They also compound their vulnerability by being active generators of reactive oxygen species (ROS) and possessing multiple substrates for oxidative damage. The major sources of ROS in these cells are their mitochondria, an L-amino acid oxidase (IL4I1) and a calcium-dependent NADPH oxidase (NOX5). Spermatozoa tolerate the risks associated with ROS generation because their biology is heavily dependent on redox regulation. ROS are important mediators of sperm capacitation, stimulating the generation of cAMP and prostaglandins, inhibiting protein phosphatases and encouraging removal of cholesterol from the plasma membrane. Furthermore, during fertilization, the ability of ROS to activate metalloproteinases facilitates penetration of the zona pellucida and sperm–oocyte fusion. While ROS are physiologically important for sperm function, the over-production of these metabolites can impair sperm function. Antioxidants have therefore assumed some importance as a possible therapy for the infertile male. However, before this potential can be realized, we need to optimize the composition and dose of reagents used in such formulations and develop improved methods of diagnosing oxidative stress within the patient population. Full article

Wire arc additive manufacturing (WAAM) is an efficient, low-cost technique for fabricating large-scale metallic components and, in particular, functionally graded materials (FGMs). This review focuses on the fabrication of 316L stainless steel–Inconel 625 FGMs by arc-based WAAM processes, examining Gas Metal Arc Welding (GMAW), Gas Tungsten Arc Welding (GTAW) and Plasma Arc Welding (PAW) in terms of their microstructural outcomes, compositional control strategies, residual stress development and mechanical performance. A critical finding emerging from the reviewed literature is that direct compositional interfaces between 316L and Inconel 625 can yield superior tensile strength and ductility and lower residual stresses compared to smooth gradient strategies, owing to the formation of detrimental secondary phases such as δ-phase, Laves phase and MC carbides at intermediate iron–nickel compositions encountered only during graded builds. The potential of Submerged Arc Additive Manufacturing (SAAM) as a future high-deposition-rate alternative for large-scale FGM fabrication is also discussed. Key challenges, including dilution control, Laves phase formation, residual stress management and the corrosion characterization of the graded region, are identified, together with priority research directions for advancing the industrial adoption of arc-based FGM components. Full article

Lower-grade gliomas (LGGs) often follow a relatively protracted clinical course; however, a substantial proportion eventually undergo malignant transformation to high-grade, treatment-refractory disease. This process has traditionally been interpreted in the context of stepwise histopathologic progression and recurrent genetic alterations. Increasing evidence, however, suggests that malignant transformation is more accurately understood as an evolutionary process shaped by the interplay among epigenetic constraints, cell-state plasticity, and selective pressures. In this review, we examine current evidence supporting a model in which early LGGs, particularly isocitrate dehydrogenase (IDH)-mutant tumors, are initially maintained in relatively restricted cellular states by metabolically imposed epigenetic programs, but progressively escape these constraints under the cumulative influence of therapy, hypoxia, immune remodeling, and genomic instability. We summarize recent advances demonstrating that progression from lower-grade to high-grade disease is accompanied by cell-state transitions characterized by altered lineage identity, acquisition of stem-like features, increased proliferative capacity, and adaptation to cellular stress. We further discuss how these transitions are reinforced by microenvironmental evolution, including vascular remodeling, extracellular matrix reorganization, and changes in immune composition, thereby creating conditions that favor clonal expansion, invasion, and therapeutic resistance. Particular attention is given to longitudinal, single-cell, and spatially resolved studies, which collectively indicate that malignant transformation is not a discrete event but a continuous process of evolutionary selection and phenotypic reprogramming. Finally, we discuss the translational implications of this framework for early risk stratification, biomarker development, and mechanism-based therapeutic intervention. By reframing malignant transformation in LGGs as a process of cell-state escape under persistent selective pressure, this review aims to provide an integrated view of glioma progression and to highlight new opportunities for precision monitoring and treatment. Full article

Proteomic research in the genus Vitis has progressed from early biochemical studies of soluble proteins to high-resolution, quantitative analyses encompassing all major organs and derived products. This review provides a comprehensive synthesis of advances in grapevine and wine proteomics. In leaves, studies have revealed extensive remodeling of photosynthetic, antioxidant, and defense pathways under biotic (e.g., Plasmopara viticola, Erysiphe necator, Xylella fastidiosa, Candidatus Phytoplasma vitis) and abiotic stresses (drought, salinity, heat, light). Bud proteomics elucidated hormonal regulation and mechanisms of dormancy release, while root studies identified nitrate-dependent metabolic shifts and adaptive protein networks. Cell culture models enabled controlled investigation of elicitor responses, stilbene biosynthesis, and temperature-induced proteome changes. In berries, proteomics clarified developmental transitions from fruit set to ripening, emphasizing proteins related to secondary metabolism, vacuolar transport, and stress tolerance. Comparative analyses across cultivars and environments identified biomarkers linked to aroma, color, and texture. The wine proteome revealed selective persistence of grape-derived proteins (e.g., thaumatin-like proteins, chitinases) and yeast peptides influencing stability and sensory properties, while Botrytis cinerea infection significantly alters this balance by degrading PR proteins and introducing fungal enzymes. Altogether, the Vitis proteome emerges as a dynamic, multifunctional system crucial for understanding plant adaptation, enological quality, and biomarker discovery. Full article

Deciphering the dynamic fracture evolution of rock masses, particularly the interaction between dynamic stress waves and localised weak interlayers, is essential for optimising dynamic rock excavation in mining engineering. To systematically explore how these structural planes halt propagating cracks and generate a dynamic shielding effect, this study integrated Split Hopkinson Pressure Bar experiments, Digital Image Correlation techniques, and computational modeling. The findings demonstrate that altering the geometric orientation of the soft layer dictates the ultimate failure pattern. While an orthogonal interface (i.e., an interface with 0° inclination perpendicular to the loading direction) allows a tension-driven crack to cleave directly through the entire composite specimen, introducing an inclined obliquity of 15° forces the advancing fracture to deviate and permanently halt inside the soft stratum. Macroscopically, this barrier capability is validated by a rapid decrease in fracture speed, which drops abruptly by 75.5% upon encountering the inclined zone. Microscopic numerical evaluations confirm that this fracture arrest originates from wave mode conversion at the misaligned boundary. The angled interface forces incoming compressional pulses to transform into intense shear stresses, promoting extensive fracture. Substantial energy dissipation within the interlayer fully deprives the primary crack of the tensile stress required for propagation, effectively confining the stress-propagated hard rock within an energy shadow zone and suppressing further fragmentation. Full article

Prominin-1 (Prom1/CD133) has long been recognized as a structural determinant of photoreceptor outer segment (OS) morphogenesis, yet rapidly accumulating evidence extends its role to retinal pigment epithelium (RPE) homeostasis, encompassing autophagy–lysosomal flux, outer segment phagocytosis, mitochondrial function, and regulation of inflammatory stress. This review synthesizes mechanistic and transcriptomic insights that position PROM1 as a central regulator of photoreceptor and RPE integrity, reframing Prom1 disease as a multi-compartment retinal disorder relevant to both inherited retinal dystrophies (IRDs) and atrophic age-related macular degeneration (aAMD). We develop a dual-axis conceptual model in which Prom1 dysfunction can initiate pathology in either the photoreceptors (OS morphogenesis failure) or the RPE, including impaired autophagic flux, lysosomal activity, defective phagocytosis, and Epithelial-Mesenchymal Transition (EMT)-like de-differentiation, with secondary cross-compartmental degeneration. Clinically, autosomal-dominant missense variants associate with macular or cone-rod dystrophy, whereas biallelic truncating/splice-site mutations drive early-onset rod–cone disease and panretinal/RPE atrophy, illustrating genotype–phenotype diversity. By integrating recent high-resolution transcriptomic data from Prom1-deficient RPE cells with long-standing insights into photoreceptor biology, we highlight converging pathways of degeneration that challenge a photoreceptor-centric view and unify disparate phenotypes within a single molecular framework. These insights broaden the therapeutic landscape, advancing gene augmentation and pathway-targeted strategies to preserve RPE integrity, sustain photoreceptor function, and modify disease course in PROM1-associated IRDs and atrophic AMD. Full article