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Background Broad bean wilt virus 2 (BBWV2) represents a major constraint on pepper cultivation, yet the molecular basis of host resistance remains poorly understood. To address this gap, we investigated the antiviral defense responses of the Xunhua pepper landrace by integrating transcriptomic, metabolomic, and physiological analyses. Results BBWV2 infection markedly altered multiple physiological parameters, including soluble sugar content, peroxidase (POD) activity, alanine aminotransferase (ALT) activity, and jasmonic acid (JA) levels, reflecting perturbations in energy metabolism, oxidative stress, and hormonal regulation. Transcriptome profiling revealed persistent activation of the MAPK signaling cascade, characterized by the upregulation of MPK7 , MAPKKK18 , WRKY22 , PR1 , and ACS1–6 , alongside the consistent downregulation of MPK4 , WRKY24 , PYL1–4 , and CTR1 , suggesting viral interference with immune signaling. Metabolomic analyses indicated pronounced enrichment in flavonoid, phenylpropanoid, and lignan biosynthetic pathways. Notably, antiviral metabolites such as aristolochic acid B, angelicin, and 7-demethylsuberosin accumulated progressively in parallel with the induction of biosynthetic genes including CHS , CHI , and PAL , supporting a coordinated transcriptional–metabolic defense response. Integrative analysis further highlighted a putative MAPK–transcription factor–metabolite regulatory axis, which may be disrupted by BBWV2 to undermine host immunity. Conclusion This study provides a comprehensive overview of the antiviral responses in pepper, underscoring the critical contributions of MAPK signaling, secondary metabolic pathways, and physiological regulation. The key candidate genes and metabolites identified herein represent promising targets for future resistance breeding and functional validation.

Surgical resection is an important avenue for cancer treatment, which, in most cases, can effectively alleviate the patient symptoms. However, accumulating evidence has documented that surgical resection potentially enhances metastatic seeding of tumor cells. In this review, we revisit the literature on surgical stress, and outline the mechanisms by which surgical stress, including ischemia/reperfusion injury, activation of sympathetic nervous system, inflammation, systemically hypercoagulable state, immune suppression and effects of anesthetic agents, promotes tumor metastasis. We also propose preventive strategies or resolution of tumor metastasis caused by surgical stress.

The morbidity and mortality of autoimmune diseases (Ads) have been increasing worldwide, and the identification of novel therapeutic strategies for prevention and treatment is urgently needed. Sirtuin 1 (SIRT1), a member of the class III family of nicotinamide adenine dinucleotide (NAD + )-dependent histone deacetylases, has been reported to participate in the progression of several diseases. SIRT1 also regulates inflammation, oxidative stress, mitochondrial function, immune responses, cellular differentiation, proliferation and metabolism, and its altered functions are likely involved in Ads. Several inhibitors and activators have been shown to affect the development of Ads. SIRT1 may represent a novel therapeutic target in these diseases, and small molecules or natural products that modulate the functions of SIRT1 are potential therapeutic agents. In the present review, we summarize current studies of the biological functions of SIRT1 and its role in the pathogenesis and treatment of Ads.

Riz1 knockout mice demonstrated obesity with activation of the V-Akt murine thymoma viral oncogene homolog (PKB) (AKT)/mechanistic target of rapamycin (mTOR) pathway. Whether the decrease in RIZ1 and the activation of AKT/mTOR exist in pregnant women with obesity is still unknown. This study examined the association between RIZ1, AKT/mTOR, and obesity through a prospective methodological approach in pregnant women. A total of 260 pregnant women, including 71 lean, 75 normal weight, 56 overweight, and 58 obesity, were enrolled. Pregnant women with obesity had higher baby weights and cesarean section rates, exhibiting the highest rate of irregular meal habits with high-protein and low-vegetable/fruit dietary patterns. The plasma concentration of C0-C5 carnitine decreased gradually from the lean to the obesity group, while the levels of amino acids and C6-C26 carnitines accumulated in overweight individuals. The expression of RIZ1 was reduced in overweight and obesity groups accompanied by AKT/mTOR activation. In addition, RIZ1 inhibited cellular adipogenesis as well as AKT/mTOR molecules in 3T3-L1 cell. This study presented comprehensive data on maternal and fetal characteristics, inhibited RIZ1, and activated AKT/mTOR molecules in pregnant women with overweight and obesity, providing valuable insights into underlying mechanisms of gestational obesity.

Pyroptosis, systemic inflammation, and mitochondrial apoptosis are the three primary contributors to sepsis's multiple organ failure, the ultimate cause of high clinical mortality. Currently, the drugs under development only target a single pathogenesis, which is obviously insufficient. In this study, an acid‐responsive hollow mesoporous polydopamine (HMPDA) nanocarrier that is highly capable of carrying both the hydrophilic drug NAD+ and the hydrophobic drug BAPTA‐AM, with its outer layer being sealed by the inflammatory targeting peptide PEG‐LSA, is developed. Once targeted to the region of inflammation, HMPDA begins depolymerization, releasing the drugs NAD+ and BAPTA‐AM. Depletion of polydopamine on excessive reactive oxygen species production, promotion of ATP production and anti‐inflammation by NAD+ replenishment, and chelation of BAPTA (generated by BA‐AM hydrolysis) on overloaded Ca2+ can comprehensively block the three stages of sepsis, i.e., precisely inhibit the activation of pyroptosis pathway (NF‐κB‐NLRP3‐ASC‐Casp‐1), inflammation pathway (IL‐1β, IL‐6, and TNF‐α), and mitochondrial apoptosis pathway (Bcl‐2/Bax‐Cyt‐C‐Casp‐9‐Casp‐3), thereby restoring intracellular homeostasis, saving the cells in a state of “critical survival,” further reducing LPS‐induced systemic inflammation, finally restoring the organ functions. In conclusion, the synthesis of this agent provides a simple and effective synergistic drug delivery nanosystem, which demonstrates significant therapeutic potential in a model of LPS‐induced sepsis. Depletion of excessive reactive oxygen species, replenishment of nicotinamide adenine dinucleotide (NAD+), and chelation of overloaded Ca2+ can comprehensively block the three stages of sepsis, saving the cells in a state of “critical survival”, further restoring the organ functions of sepsis mice.

The aim of this study was to systematically evaluate the independent efficacy of platelet-rich fibrin (PRF) as a sole grafting material in alveolar ridge preservation and to dynamically delineate the trajectory of PRF's effects on alveolar ridge morphology and new bone formation across various healing stages. A comprehensive search was conducted across four databases (PubMed, Embase, the Cochrane Library, and Web of Science) for pertinent records from their establishment until November 2025. The study encompassed randomized controlled trials (RCTs) that evaluated alveolar ridge preservation utilizing PRF alone in comparison to spontaneous healing. Two investigators independently conducted literature screening, data extraction, and methodological quality evaluation, employing the Cochrane Risk of Bias instrument (ROB-2) for the latter. The certainty of the evidence for each outcome was assessed using the GRADE framework. The meta-analysis utilized RevMan version 5.3, while publication bias was evaluated by Egger's test in Stata 18. A total of eighteen studies were incorporated into the analysis. Compared to the spontaneous healing group, the PRF group showed significantly smaller losses in alveolar bone height at 3 months (  = 0.004; 95% CI = -1.59 to -0.31), 4 months (  = 0.002; 95% CI = -0.93 to -0.20), and 6 months (  = 0.03; 95% CI = -0.53 to -0.03). The use of PRF resulted in a significantly lower reduction in alveolar bone width at 2 months (  = 0.03; 95% CI = -1.18 to -0.05) and 3 months. The percentage of new bone formation in the PRF group was significantly greater than that in the spontaneous healing group at both 3 months (  = 0.0008; 95% CI: 4.70-18.02) and 4 months (  = 0.010; 95% CI: 4.14-29.81). High-speed centrifugation was associated with significantly greater new bone formation than standard protocols (  = 0.02), while effects on dimensional preservation did not differ significantly between protocols. PRF appears to mitigate alveolar bone resorption following tooth extraction and may enhance new bone formation during the healing process. The osteogenic effect of PRF may be optimized by high-speed centrifugation protocols. As a secure autologous biomaterial, it is a promising option for preserving alveolar bone and enhancing circumstances for eventual implant restoration. https://www.crd.york.ac.uk/PROSPERO/view/CRD420251183872, identifier PROSPERO (CRD420251183872).

Cyclic peptides have attracted tremendous attention in the pharmaceutical industry owing to their excellent cell penetrability, stability, thermostability, and drug-like properties. However, the currently available facile methodologies for creating such peptides are rather limited. Herein, we report an efficient and direct peptide cyclization via rhodium(III)-catalyzed C(7)-H maleimidation. Notably, this catalytical system has excellent regioselectivity and high tolerance of functional groups which enable late-stage cyclization of peptides. This architecture of cyclic peptides exhibits higher bioactivity than its parent linear peptides. Moreover, the Trp-substituted maleimide displays excellent reactivity toward Michael addition, indicating its potential as a click functional group for applications in chemical biology and medicinal chemistry. As a proof of principle, RGD-GFLG-DOX, which is a peptide-drug-conjugate, is constructed and it displays a strong binding affinity and high antiproliferative activity toward integrin-αvβ 3 overexpressed cancer cell lines. The proposed strategy for rapid preparation of stapled peptides would be a robust tool for creating peptide-drug conjugates. Cyclic peptides are of interest due to their application in pharmaceutical industry, but currently there are limited methodologies for their synthesis. Here, the authors report an efficient and direct peptide cyclization via rhodium(III)-catalysed C(7)-H maleimidation.

Background As a popular and valuable technique, grafting is widely used to protect against soil-borne diseases and nematodes in vegetable production. Growing evidences have revealed that long intergenic ncRNAs (lincRNAs) are strictly regulated and play essential roles in plants development and stress responses. Nevertheless, genome-wide identification and function deciphering of pepper lincRNAs, especially for their roles in improving grafting pepper resistance to Phytophthora capsici is largely unknown. Results In this study, RNA-seq data of grafting and control pepper plants with or without P . capsici inoculation were used to identify lincRNAs. In total, 2,388 reliable lincRNAs were identified. They were relatively longer and contained few exons than protein-coding genes. Similar to coding genes, lincRNAs had higher densities in euchromatin regions; and longer chromosome transcribed more lincRNAs. Expression pattern profiling suggested that lincRNAs commonly had lower expression than mRNAs. Totally, 607 differentially expressed lincRNAs (DE-lincRANs) were identified, of which 172 were found between P . capsici resistance grafting pepper sample GR and susceptible sample LDS. The neighboring genes of DE-lincRNAs and miRNAs competitively sponged by DE-lincRNAs were identified. Subsequently, the expression level of DE-lincRNAs was further confirmed by qRT-PCR and regulation patterns between DE-lincRNAs and neighboring mRNAs were also validated. Function annotation revealed that DE-lincRNAs increased the resistance of grafting prepper to P . capsici by modulating the expression of disease-defense related genes through cis -regulating and/or lincRNA-miRNA-mRNA interaction networks. Conclusions This study identified pepper lincRNAs and suggested their potential roles in increasing the resistance level of grafting pepper to P . capsici .

Highland barley is one of the few crops that can be grown at high elevations, making it a key resource within the Tibet Plateau. Weeds are a significant threat to highland barley production, and new herbicides and tolerant barley varieties are needed to control this ever-growing problem. A better understanding of existing herbicide resistance mechanisms is therefore needed. In this study, transcriptomic and metabolomic analyses were used to identify molecular and physiological changes in two highland barley genotypes with differing sensitivities to the herbicide pyroxsulam. We identified several stress-responsive metabolites, including flavonoids and antioxidants, which accumulated to significantly higher levels in the pyroxsulam-resistant genotype. Additionally, we found key genes in both the flavonoid biosynthesis pathway and the antioxidant system that were up-regulated in pyroxsulam-resistant barley. This work significantly expands on the current understanding of the molecular mechanisms underlying differing pyroxsulam tolerance among barley genotypes and provides several new avenues to explore for breeding or engineering tolerant barley.

Rheumatoid arthritis (RA) is an autoimmune inflammatory disease, of which the leading cause of death is cardiovascular disease (CVD). The levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-c), and high-density lipoprotein cholesterol (HDL-c) in RA decrease especially under hyperinflammatory conditions. It is conflictive with the increased risk of CVD in RA, which is called “lipid paradox”. The systemic inflammation may explain this apparent contradiction. The increased systemic proinflammatory cytokines in RA mainly include interleukin-6(IL-6)、interleukin-1(IL-1)and tumor necrosis factor alpha(TNF-α). The inflammation of RA cause changes in the subcomponents and structure of HDL particles, leading to a weakened anti-atherosclerosis function and promoting LDL oxidation and plaque formation. Dysfunctional HDL can further worsen the abnormalities of LDL metabolism, increasing the risk of cardiovascular disease. However, the specific mechanisms underlying lipid changes in RA and increased CVD risk remain unclear. Therefore, this article comprehensively integrates the latest existing literature to describe the unique lipid profile of RA, explore the mechanisms of lipid changes, and investigate the impact of lipid changes on cardiovascular disease.