Search Results (12,500)

Camellia oleifera Abel. is a typical self-incompatible plant, yet its molecular mechanisms have not been comprehensively elucidated, which constitutes the principal cause underlying the relatively low natural fruit set rate in C. oleifera. S-RNase belongs to the RNase T2 gene family and represents a class of glycoproteins specifically expressed in the style with certain “cytotoxicities” capable of degrading ribonucleic acid (RNA) in their own pollen tube cells, thereby inducing programmed cell death in pollen tube cells. To identify pistil S genes participating in the self-incompatibility response of C. oleifera, nine RNase T2 family genes were identified based on transcriptomic and whole-genome sequencing data of the camellia oil tree and designated CoRNS1–CoRNS9. Systematic evolutionary analysis revealed that CoRNS5, CoRNS7, and CoRNS8 exhibit close phylogenetic relationships with S-RNases of the Camelliaceae family, whereas CoRNS6 shows closer affinity with S-RNases of the Solanaceae family. Analysis of promoter cis-acting elements revealed that RNase T2 family genes are regulated by multiple hormones, including abscisic acid, methyl jasmonate, cytokinin, auxin, salicylic acid, and gibberellin, and possess MYB transcription factor-binding sites. Expression analysis revealed that CoRNS6 is expressed exclusively in the ovary; CoRNS5 is expressed at the highest level in the style, followed by lower levels in the petals, anthers, filaments, receptacle, and ovary; CoRNS1 is expressed in all tissues except anthers; and the other genes are expressed across various floral tissues. Ex vitro pollen culture system experiments demonstrated that the CoRNS1 and CoRNS5 recombinant proteins significantly inhibited the elongated growth of autogamous pollen tubes, whereas CoRNS7 significantly reduced the pollen germination rate. Fluorescence labeling revealed that treatment of autogamous pollen tubes with the recombinant proteins CoRNS1, CoRNS5, and CoRNS7 induced microfilament skeleton depolymerization and increased the Ca²⁺ concentration within the pollen tubes. Additionally, treatment with the CoRNS5 recombinant protein increased the reactive oxygen species (ROS) levels in autogamous pollen tubes. These findings suggest that RNase T2 family genes are involved in the self-incompatibility response in C. oleifera, with CoRNS1, CoRNS5, and CoRNS7 playing pivotal roles. Overall, our results not only offer a theoretical foundation for elucidating the regulatory network governing self-incompatibility in C. oleifera, but also furnish valuable genetic resources for future molecular breeding programs targeting improved self-compatibility and increased fruit yield. Full article

Reactive oxygen species (ROS) exert dual biological functions in plants. Though they form toxic byproducts of aerobic metabolism, ROS also serve as indispensable secondary messengers that orchestrate stress acclimation programs. For decades, plant physiologists operated under a pervasive assumption that constitutive and non-compartmentalized upregulation of antioxidant capacity would universally enhance abiotic stress tolerance. This long-standing dogma has now been thoroughly overturned. A growing body of evidence shows that sustained, global high antioxidant activity often impairs adaptation rather than helping it. In this review, we replace the simplistic “more antioxidants equal better tolerance” framework with a dynamic model of cellular redox homeostasis. We dissect three interconnected mechanisms though which unrestrained ROS scavenging generates deleterious phenotypic outcomes. First, indiscriminate clearance blunts transient ROS pulses and propagating ROS waves, the core signaling events acquired to trigger systemic acquired acclimation (SAA). Second, continuous antioxidant biosynthesis drains finite carbon skeletons, NADPH, and ATP pools, exacerbating evolutionary growth-defense resource trade-offs. Third, non-specific bulk ROS scavenging erases compartment-specific organellar retrograde signals, which rely on tightly controlled spatial and temporal ROS fluctuations. We concurrently define physiological boundary conditions where robust antioxidant activity remains vital for plant survival under extreme stress. Rather than advocating for the complete suppression of ROS detoxification, our analysis advocates context-dependent fine-tuning of redox signaling networks. We also summarize emerging precision redox monitoring and genetic engineering tools, and outline translational breeding pipelines to develop climate-resilient crops that balance stress survival and yield stability. This work delivers novel conceptual perspectives to advance fundamental plant redox biology. Full article

Iron oxychloride (FeOCl) has recently attracted considerable attention as a high-performance heterogeneous Fenton-like catalyst. Its layered Fe-O-Cl coordination environment enables rapid FeIII/FeII redox cycling and efficient activation of H₂O₂, thereby promoting the generation of reactive oxygen species (ROS) for pollutant degradation. This review summarizes recent progress in FeOCl-based materials, including their crystal structure, optical, electrochemical, magnetic and other physicochemical properties, synthesis strategies, catalytic mechanisms, and environmental applications, with particular emphasis on experimental evidence and density functional theory (DFT) calculations. Special attention is given to pH-insensitive H₂O₂ activation, visible-light-assisted Fenton-like reactions, heterojunction construction, elemental doping, intercalation engineering, membrane-supported catalysts, morphology engineering, and flow-through electro-Fenton configurations. FeOCl-based catalysts have demonstrated outstanding performance in degrading dyes, antibiotics, phenolic compounds, endocrine-disrupting compounds, and other recalcitrant pollutants, while also showing potential in heavy-metal adsorption, selective oxidation, and energy-related applications. Finally, remaining challenges concerning catalyst stability, iron leaching, scalable synthesis, realistic water matrices, byproduct toxicity, and reactor integration are discussed to guide the rational design of practical FeOCl-based catalytic systems. Full article

Sepsis-induced cardiomyopathy (SICM) is a life-threatening complication of sepsis; however, its molecular mechanisms remain incompletely understood, which has hindered the development of targeted therapies. We hypothesized that excessive mitochondrial reactive oxygen species (mtROS) production through reverse electron transfer (RET) at mitochondrial complex I contributes to septic myocardial injury and that metformin, a clinically used inhibitor of mitochondrial complex I, protects the myocardium by inhibiting this process. In lipopolysaccharide-stimulated H9C2 cardiomyocytes and cecal ligation and puncture-induced septic rats, sepsis was characterized by an elevated mitochondrial membrane potential, accompanied by succinate accumulation, an increased NADH/NAD⁺ ratio, and impaired downstream electron transport. These metabolic changes established favorable conditions for RET-mediated mtROS generation. Metformin inhibited complex I activity and selectively suppressed RET-mediated mtROS generation without increasing ROS production associated with forward electron transport (FET). This effect was accompanied by attenuated inflammatory responses and apoptosis. In septic rats, metformin preserved cardiac function and alleviated myocardial oxidative stress and injury. Overall, these results suggest that RET at mitochondrial complex I represents a potential therapeutic target in SICM and support the use of metformin as a promising strategy for preventing and treating septic myocardial dysfunction. Full article

Background: CAV (cardiac allograft vasculopathy) is considered the leading cause of late post-transplant mortality and affects approximately 50% of transplant patients at 10 years post-transplant. Its etiopathogenetic mechanism is considered to be immune-mediated, but the identification of other non-immunological risk factors could represent new therapeutic targets for this pathology. Lipofuscin is due to reactive oxygen species (ROS) and appears to have a determining role in CAV. The aim of this study is to investigate the association between the amount of lipofuscin identified on EMB (endomyocardial biopsy) from patients followed up after heart transplantation, and the presence of CAV detected by coronary angiography. Methods: This retrospective study includes 99 EMBs from 47 transplanted patients, who also had coronary angiography. The amount of lipofuscin, damage to intramyocardial small vessels, vasculitis, Quilty effect, and acute cellular and humoral rejection was evaluated microscopically. Results: 19 CAV cases (19.2%) were identified, of which 15 (68.18% of total CAV cases) were insignificant. Grade 3 lipofuscin affected equally the cases with insignificant and significant CAV, 3 cases (37.5%) from each group. Grade 2 lipofuscin was reported in 10 cases (58.8%) of insignificant CAV, respectively 1 case of significant CAV (5.9%), (p-value of 0.0001). Quantitative evaluation of lipofuscin on microscopic sections revealed 8 EMBs (8.1%) with grade 3 lipofuscin. Two cases (25.0%) with lipofuscin score 3 were associated with moderate ACR (acute cellular rejection), ISHLT 2R and 3 cases (37.5%) with lipofuscin score 3 were associated with mild ACR ISHLT 1R, the differences being statistically significant, (p = 0.0001). Lipofuscin grades 2 and 3 were associated with severe fibrosis in 6 cases (35.3%) and 2 cases (25.0%), respectively (p = 0.042). A statistically significant association between the degree of damage to the intramyocardial small vessels and the amount of intracytoplasmic lipofuscin was observed (p = 0.00014). Discussion: Our study revealed that lipofuscin was more frequently associated with CAV, fibrosis, and damaged small vessels. Oxidative stress influences lipofuscinogenesis and CAV, which leads to endothelial dysfunction and neointimal hyperplasia, which over time will produce progressive narrowing of the vascular lumen and dysfunction of the cardiac allograft. Of the total number of 19 cases with CAV, 17 (89.47%) presented a lipofuscin score of 2 or 3 concomitantly with CAV, (p = 0.0001). This could mean that lipofuscin is not a harmless degradation product. At the same time, the association of a large number of cases with lipofuscin score 2, 10 cases (58.8%) with insignificant CAV could lead to the idea of using lipofuscin as a potential biomarker in the early diagnosis of CAV. Conclusions: We evidenced a significant association between the amount of intracytoplasmic lipofuscin and CAV. Accordingly, lipofuscin might be involved in the pathogenesis of CAV. Further research is needed to clarify the exact mechanisms of this association. Full article

Reactive oxygen species (ROS) regulate cellular signaling at physiological concentrations and drive tissue damage when their generation exceeds antioxidant defenses. The conceptual reframing of the field into oxidative eustress (low, controlled redox signaling) and oxidative distress (supraphysiological levels causing biomolecular damage), alongside parallel advances in detection chemistry and genetically encoded biosensors, has transformed how investigators measure ROS in living systems. This review provides a critical, methods-focused update covering the contemporary toolkit, with particular emphasis on advances from 2015 to 2026 while incorporating earlier foundational work where it remains indispensable to interpretation. Consistent with the title and reflecting both the maturity of the available chemistry and the weight of the recent literature, our emphasis falls on hydrogen peroxide and mammalian experimental systems; superoxide, the hydroxyl radical, and singlet oxygen are addressed primarily where their detection intersects with the platforms reviewed here, and non-mammalian models are considered only selectively. Readers seeking dedicated coverage of these other species or of plant, microbial, and invertebrate systems are directed to the specialized reviews cited throughout. Five complementary measurement platforms are evaluated: (i) electron paramagnetic resonance spectroscopy with classical nitrone spin traps and the newer cyclic hydroxylamine probes; (ii) small-molecule fluorescent probes, with particular emphasis on the boronate-based, activity-based sensing platform that has supplanted 2′,7′-dichlorofluorescin diacetate for hydrogen peroxide imaging; (iii) genetically encoded biosensors of the HyPer and roGFP families, which now permit ratiometric, organelle-resolved, and longitudinal measurements; (iv) mass-spectrometry-based quantification of oxidation products and radical adducts, including isoprostanes, 2-hydroxyethidium, and redox-modified cysteines via chemical proteomics; and (v) electrochemical and nanosensor approaches enabling real-time single-cell measurements. The selectivity, sensitivity, temporal resolution, spatial resolution, and quantitative capability of each platform are critically compared. Reliance on a single non-specific probe is no longer sufficient as the sole evidence base for quantitative or species-specific claims; contemporary investigators are expected to apply complementary approaches and to validate findings across modalities. Standardization of reporting, integration with single-cell omics, and clinical translation of validated mass-spectrometry biomarkers are identified as priorities for the coming decade. Full article

Reactive oxygen species (ROS) are central regulators of cancer biology and represent a double-edged target in oncology. At physiological levels, ROS support signal transduction, proliferation, differentiation, and immune responses, whereas sustained ROS imbalance promotes DNA damage, genomic instability, metabolic reprogramming, and remodeling of the tumor microenvironment, thereby contributing to tumor initiation, progression, metastasis, and therapy resistance. Conversely, because many cancer cells operate close to the limit of tolerable oxidative stress, further ROS elevation can trigger apoptosis, ferroptosis, immunogenic cell death, and other cytotoxic programs. This review summarizes the major intracellular and microenvironmental sources of ROS, the mechanisms by which redox signaling shapes malignant transformation and tumor adaptation, and the antioxidant systems that buffer oxidative stress in cancer cells. We further discuss current therapeutic approaches based on both ROS suppression and ROS amplification, including redox-modulating small molecules, radiotherapy, photodynamic and sonodynamic therapy, catalytic nanomaterials, and ROS-responsive prodrugs and drug delivery systems. Particular attention is given to the context-dependent effects of ROS, the antioxidant paradox, tumor heterogeneity, hypoxia, off-target toxicity, and the need for robust redox biomarkers. A deeper understanding of tumor-specific redox vulnerabilities will be essential for developing precise and clinically effective ROS-oriented cancer therapies. Full article

Tanacetum cinerariifolium (pyrethrum) is a commercially valuable ornamental and economically important industrial crop that produces pyrethrins, a mixture of six insecticidal esters with potent insecticidal activity and a relatively low toxicity to mammals. Drought stress is a major constraint on pyrethrum cultivation, impairing vegetative growth and leaf physiological function. However, the effects of drought on pyrethrin biosynthesis and the underlying drought-response mechanisms remain poorly understood. In this study, we investigated drought-induced changes in pyrethrum leaves through integrated phenotypic observation, physiological and biochemical analyses, and transcriptome sequencing. Drought stress caused leaf dehydration, wilting, and chlorosis, accompanied by increased activities of antioxidant enzymes, including superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT), together with enhanced proline accumulation, indicating the activation of reactive oxygen species (ROS) scavenging and osmotic adjustment. Under severe drought stress, membrane lipid peroxidation increased further, indicating damage to cellular integrity. Transcriptomic analysis revealed extensive drought-induced transcriptional reprogramming in pyrethrum leaves, with the number of differentially expressed genes increasing as the stress severity increased. Abscisic acid (ABA) biosynthesis pathway was significantly activated, with 9-cis-epoxycarotenoid dioxygenase 3 (NCED3) strongly upregulated under severe drought stress, whereas NCED9 and abscisic aldehyde oxidase 3 (AAO3) were primarily responsive to mild drought stress and downregulated under severe conditions. Concurrently, the pyrethrin biosynthesis pathway was partially inhibited, indicating that pyrethrum prioritizes ABA-mediated drought tolerance over pyrethrin production. These findings provide insight into drought-induced physiological and transcriptional responses and may inform the development of drought-tolerant pyrethrum germplasm with an enhanced quality. Full article

Soil salinity is a major environmental constraint that threatens global food security by significantly inhibiting seed germination and early seedling establishment. Salinity disrupts all three phases of seed germination: Phase I (imbibition), where reduced water absorption capacity reduces seed hydration and delays metabolic reactivation; Phase II (lag phase), where ionic toxicity and oxidative stress impair enzyme activity, reserve mobilization, and cellular metabolism; and Phase III (radicle protrusion), where limited cell division and length prevent radicle emergence and seedling establishment. These disturbances reduce germination percentage, germination rate, germination index, germination energy, and plant vigor, while increasing average germination time. At the morpho-physiological level, salinity impairs water absorption, membrane stability, photosynthetic pigment accumulation, and root–shoot development. Biochemically, excessive accumulation of reactive oxygen species (ROS), hydrogen peroxide (H₂O₂), and malondialdehyde (MDA) causes cellular damage and metabolic dysfunction. At the molecular level, salinity alters the expression of the aquaporin gene family (PIPs, TIPs, NIPs, and SIPs), suppresses starch mobilization by reducing α-amylase, enhances abscisic acid (ABA) signaling, and inhibits gibberellic acid (GA) biosynthesis, all of which cause inhibition of germination and early growth. As a result, an effective strategy is needed to improve seed germination under saline conditions. Therefore, the second focus of this review is to critically evaluate the potential of nanoparticles (NPs) and nanobiochar (NBC) as emerging tools to mitigate salinity stress during seed germination. Current evidence suggests that NPs and NBC enhance water absorption, maintain membrane strength, improve nutrient availability, promote antioxidant defense systems, and regulate osmotic adjustment in saline environments. Furthermore, these nanomaterials alter key molecular pathways involved in aquaporin expression, hormonal homeostasis, and reserve mobilization, thereby promoting successful germination and seedling establishment. By combining recent advances in physiological, biochemical, and molecular research, this review provides a comprehensive understanding of salinity-induced germination disruption and highlights the potential of NP- and NBC-based approaches to improve crop establishment under saline conditions. Full article

Ascorbate (AsA), or vitamin C, is a central redox metabolite that functions as an antioxidant, enzyme cofactor, and electron donor. Its cellular function depends not only on biosynthesis or dietary uptake, but also on rapid recycling from its oxidized forms, monodehydroascorbate (MDHA) and dehydroascorbate (DHA). This requirement is especially evident in high-demand systems such as plant chloroplasts, which face continuous photosynthetic reactive oxygen species (ROS) production under illumination, and human neutrophils, which accumulate millimolar ascorbate to withstand NADPH oxidase-driven oxidative bursts in pathogen defense. Here, we revisit ascorbate recycling from a sulfur-centered perspective. Historical studies of plant, animal, and solution-chemistry pathways show that many DHA-reducing systems converge on sulfur chemistry, including glutathione (GSH), cysteine-dependent enzymes, H₂S, and modified thiols. We propose that ascorbate recycling is organized as a multilayered system in which nonenzymatic reactions are accelerated by enzymes, localized within cellular or extracellular compartments, and integrated with broader NAD(P)H-, glutathione-, sulfur-, and diet-dependent redox networks. Within this framework, the AsA/DHA couple can be viewed as a molecular redox capacitor that buffers transient oxidative pressure. Reactive sulfur species (RSS), including persulfides and polysulfides, represent chemically plausible but experimentally unresolved contributors to DHA reduction. Full article

Bisphenols are a family of synthetic endocrine-disrupting compounds commonly found in water systems, where they persist because of the limitations of conventional wastewater treatment. Nanomaterial-based Advanced Oxidation Processes (AOPs) have been widely studied as promising approaches for bisphenol degradation, achieving high removal efficiencies by generating reactive oxygen species (ROS). However, incomplete mineralization frequently leads to the formation of transformation products, which may have toxicological characteristics that differ significantly from those of the parent compounds. This review focuses on the toxicity of the degradation products generated during the nanomaterial-based AOP treatment of bisphenol A (BPA), bisphenol S (BPS), bisphenol F (BPF), and bisphenol AF (BPAF). Evidence from ecotoxicological, phytotoxicological, cytotoxic, genotoxic, neuroactive, and endocrine disruption studies shows that some intermediates may display toxicity equal to or exceeding that of the parent compounds, particularly during intermediate treatment stages. The influence of operational parameters such as catalyst type, ROS composition, irradiation conditions, and treatment duration on transformation product (TP) formation and toxicity evolution was further investigated. These findings suggest that removing the parent compound is not enough to guarantee the environmental safety of treated effluents and stress the importance of including a comprehensive toxicological assessment when evaluating advanced water treatment technologies. Full article

Histone deacetylases (HDACs) are key epigenetic enzymes governing lysine deacetylation. This modification is tightly coupled to cellular redox homeostasis and antioxidant signaling in plants. Plant HDACs are grouped into three subfamilies: RPD3/HDA1, SIR2, and plant-specific HD2. HDACs target both histone residues (e.g., H3K9 and H4K5) and a broad set of non-histone substrates (e.g., transcription factors and metabolic enzymes). Via coordinated chromatin remodeling and non-histone protein modification, HDACs integrate phytohormone signals, reactive oxygen species (ROS) bursts and NAD⁺ metabolic fluctuations to orchestrate plant abiotic stress responses, balancing antioxidant defense, redox equilibrium and normal growth. This review systematically sorts the divergent stress-response traits, substrate preferences and bidirectional regulatory logic of the three HDAC subfamilies; integrates chromatin-dependent and transcription factor-centered transcriptional branches; and summarizes crosstalk rules between HDAC-mediated deacetylation and other epigenetic marks. We further hierarchically clarify current research bottlenecks spanning basic mechanism dissection, multi-crop validation and field breeding transformation and propose targeted stratified research directions. We further construct a complete regulatory cascade linking environmental stimuli, ROS/ABA/NAD⁺ signals, HDAC activity and downstream antioxidant/stress gene expression, filling gaps in previous reviews that overlook redox-dependent HDAC functions. This mechanistic framework delivers integrated epigenetic and redox theoretical references for breeding stress-tolerant crops with reinforced antioxidant capacity. Full article

With the increasing prevalence of antibiotic–heavy metal co-contamination in agricultural wastewater, elucidating the antibiotic removal capacity of degrading bacteria under heavy metal stress, as well as their adaptive mechanisms, is of considerable theoretical significance and practical value. In this study, the highly efficient TYL-degrading strain TYL-A1 was selected as a model organism, and the effects of Pb²⁺ exposure on its TYL removal performance, oxidative stress response, cell surface characteristics, and transcriptional regulation were systematically investigated. The results showed that TYL removal remained above 85% after 72 h under a nominal Pb²⁺ concentration of 100 mg/L in the phosphate-containing MSM system. The phosphate may have reduced Pb²⁺ bioavailability. Nominal Pb²⁺ exposure increased the activities of superoxide dismutase (SOD) and catalase (CAT), accompanied by elevated levels of reactive oxygen species (ROS) and malondialdehyde (MDA), as well as a decrease in adenosine triphosphate (ATP) content. This indicates that the strain experienced pronounced oxidative stress and altered energy metabolism. Meanwhile, cell membrane permeability increased. Scanning electron microscopy (SEM) and Fourier-transform infrared spectroscopy (FTIR) analyses showed that the overall cellular morphology remained intact, whereas the membrane surface structure and related cellular components underwent adaptive changes. According to a transcriptomic analysis, the differentially expressed genes were mainly enriched in pathways associated with primary metabolism, transmembrane transport, ABC transporters, and two-component systems. In summary, strain TYL-A1 maintained high TYL removal performance under the tested nominal Pb²⁺ concentrations in the present phosphate-containing culture system, suggesting its potential applicability in the bioremediation of water bodies co-contaminated with antibiotics and heavy metals. Full article

Microalgae biophotovoltaic (BPV) systems convert solar energy into electricity through photosynthetic electron transfer (PET) and have emerged as a promising solar-integrated bioenergy technology. However, high-density tubular arrays suffer from the “canyon effect” at low solar angles and from photoinhibition under peak irradiance (>450 W/m²), where non-photochemical quenching (NPQ) and reactive oxygen species (ROS) dissipate bioelectric potential as heat. To address this, a hysteresis-based dual-mode PID controller with hysteresis switching is proposed within an optical–mechanical–biological co-optimization framework, integrating array self-shading, nonlinear microalgal photoresponse, and tracking parasitic losses. In low-light mode, the system actively tracks the sun to minimize shading; in peak-light mode, it defocuses the incident angle to limit irradiance near the saturation threshold, mitigating the risk of photoinhibition. Structural control boundaries, including tube spacing and connecting rod length, are determined numerically. Under the nominal clear-sky design day, the defocusing mode reduces the daily exposure of the culture to irradiance above the saturation threshold (450 W/m²) from 5.28 h to 3.08 h. Numerical simulations indicate a daily net energy yield improvement of +14.9% over continuous dual-axis tracking and +6.3% over the latitude-based fixed-tilt baseline under idealized clear-sky design-day conditions. These values are simulation-derived estimates; experimental validation with a physical prototype is required before the framework can be interpreted as a validated system-level performance gain. Full article

Petal blight caused by Neopestalotiopsis clavispora infection in Rhododendron delavayi petals severely reduces their ornamental value; however, the metabolic and transcriptional responses of petals to this pathogen remain unclear. In this study, we integrated widely targeted metabolomic and transcriptomic analyses to systematically characterize the response mechanisms of R. delavayi petals at early (1 day post-infection), middle (2 days post-infection), and late (4 days post-infection) stages of N. clavispora infection. A total of 1251 metabolites were identified, and K-means clustering analysis revealed that the differentially accumulated metabolites (DAMs) in Subclass 1 were significantly enriched in flavonoid, phenylpropanoid, and glutathione metabolic pathways. Transcriptomic analysis identified 3744, 6986, and 5407 differentially expressed genes (DEGs) at early, middle and late stages, respectively. Weighted gene co-expression network analysis (WGCNA) indicated that the key hub genes at early, middle, and late stages were mainly involved in maintaining reactive oxygen species (ROS) homeostasis, plant–pathogen interaction signal transduction, and cell wall remodeling, respectively. Joint metabolomic and transcriptomic analysis showed that phenylpropanoid, flavonoid, and glutathione pathways were commonly and significantly enriched. In vitro antifungal assays demonstrated that 2000 mg/L phloretin significantly inhibited mycelial growth of N. clavispora and effectively alleviated petal infection. Collectively, R. delavayi petals exhibit stage-specific defense strategies against N. clavispora: in the early stage, by inducing H₂O₂ accumulation and ROS homeostasis; in the middle stage, by activating immune signaling pathways; and in the late stage, by enhancing cell wall remodeling and antioxidant capacity. This study provides a theoretical basis and a candidate compound for green control of petal blight. Full article