Ulcerative colitis (UC) is a chronic idiopathic inflammatory disease affecting the colon and rectum. Characterized by recurrent attacks, UC is often resistant to traditional anti-inflammatory therapies, imposing significant physiological, psychological, and economic burdens on patients. In light of these challenges, innovative targeted therapies have become a new expectation for patients with UC. A crucial pathological feature of UC is the impairment of the intestinal mucosal barrier, which underlies aberrant immune responses and inflammation. Intestinal stem cells (ISCs), which differentiate into intestinal epithelial cells, play a central role in maintaining this barrier. Growing studies have proved that regulating the regeneration and differentiation of ISC is a promising approach to treating UC. Despite this progress, there is a dearth of comprehensive articles describing the role of ISCs in UC. This review focuses on the importance of ISCs in maintaining the intestinal mucosal barrier in UC and discusses the latest findings on ISC functions, markers, and their regulatory mechanisms. Key pathways involved in ISC regulation, including the Wnt, Notch, Hedgehog (HH), Hippo/Yap, and autophagy pathways, are explored in detail. Additionally, this review examines recent advances in ISC-targeted therapies for UC, such as natural or synthetic compounds, microbial preparations, traditional Chinese medicine (TCM) extracts and compounds, and transplantation therapy. This review aims to offer novel therapeutic insights and strategies for patients who have long struggled with UC.

Background:The pathogenesis of inflammatory bowel diseases (IBD) and their interaction with viruses have attracted growing scientific attention, as viral infections and gut virome dysregulation are increasingly recognized as key drivers of IBD onset, disease activity, and treatment responses. However, a systematic analysis of research trends in this field is lacking, leaving critical gaps in understanding how viral factors shape IBD pathogenesis and clinical management. This study conducted a bibliometric analysis to map trends, key areas, and emerging topics in the virus-IBD field from 2014 to 2024, with a focus on the pathogenic roles of viruses. The goal was to inform future research directions and bridge the gap between basic science and clinical practice. Methods:Publications related to virus-IBD were retrieved from the Web of Science Core Collection. The analysis employed VOSviewer, CiteSpace, and HistCite software to explore bibliometric dimensions, including annual publication trends, contributions by countries/regions and institutions, collaboration networks, highly cited references, citation bursts, and keyword co-occurrence and evolution. Results:Among 3,225 publications analyzed, three distinct phases were observed: fluctuating growth (2014-2019), a sharp rise (2020-2021), and a gradual decline (2022-2024). The United States (996 publications) and China (507 publications) were the dominant contributors to the field. The Mayo Clinic led in institutional publication output, while Jean-Frederic Colombel and Silvio Danese were among the most prolific and cited authors. Inflammatory Bowel Diseases and Frontiers in Immunology were leading journals. Keyword and reference analyses highlighted major research domains: gut virome mechanisms and modulation, clinical strategies for opportunistic viral infections, and IBD management during Coronavirus Disease 2019 (COVID-19). Conclusion:This study establishes an integrated knowledge framework of virus-IBD research, highlighting three essential domains: gut virome regulation and therapy, clinical management of opportunistic viral infections, and IBD care in the COVID-19 era. It further clarified the pathophysiological interplay between viral factors and IBD. By synthesizing key contributors, core themes, and evolutionary trends, this work provides a practical foundation for guiding translational research and promoting clinical innovation.

The brain, which contains high levels of catecholamines and unsaturated lipids, is particularly susceptible to oxidative damage. Against this background, increasing antioxidant levels through diet seems to be a potential approach to the prevention of neurodegenerative diseases. A recent innovative study suggests that the shape of the brain itself, rather than just the neural pathways, can have a significant impact on our cognitive processes. Here, we investigated the causal relationship between diet-derived circulating antioxidants and surface area (SA) and thickness (TH) of brain cortical structure using Mendelian randomization (MR). Published studies were used to identify instrumental variables related to absolute levels of circulating antioxidants like lycopene, retinol, ascorbate, and β-carotene, as well as antioxidant metabolites such as ascorbate, retinol, α-tocopherol, and γ-tocopherol. Outcome data on brain cortical structure were obtained from the ENIGMA consortium, which included a total of 51,665 participants. Following the guidelines of the Desikan-Killiany atlas, the cortical structure was divided into 34 regions, resulting in 70 phenotypes covering both the global and regional aspects of SA and TH. Inverse variance weighted or Wald ratio was chosen as the main method for MR analysis based on the number of single nucleotide polymorphisms. Furthermore, we performed sensitivity analyses to confirm the reliability of the findings. At the global level, absolute circulating levels of ascorbate were found to increase SA of the full cortex (β = 2244.536 mm2, 95% CI: 921.172 mm2 to 3567.901 mm2, P = .001) but had no causal relationship with TH of the full cortex (β = -0.008 mm, 95% CI: -0.020 mm to 0.005 mm, P = .228). For the levels of functional parcellation analysis, we found that circulating ascorbate metabolite significantly reduced the SA of the inferior parietal (β = -110.917 mm2; 95% CI: -176.543 mm2 to -45.292 mm2; P = .00092) and absolute circulating retinol significantly reduced the TH of the precuneus (β = -0.045 mm; 95% CI: -0.073 mm to -0.017 mm; P = .00146). No heterogeneity, pleiotropy or outliers were found. MR estimates suggest that absolute circulating levels of ascorbate increase the SA of the whole cortex. There were also 2 significant negative correlations between circulating antioxidants and cortical structure. These results provide important insights into how circulating antioxidants influence structural changes within specific cortical areas and remind us of the potential adverse consequences of supplementation with circulating antioxidants.

Background:Ulcerative colitis (UC) is a chronic inflammatory bowel (IBD) disease characterized by a complex pathogenesis and limited treatment options. Macrophages play a key role in the pathophysiology of UC by regulating inflammatory responses and tissue repair processes. Currently, there is no comprehensive summary of macrophage regulatory pathways in UC, either domestically or internationally. Objective:This review aims to systematically elucidate the role of macrophages in UC and their specific regulatory mechanisms, and to identify potential therapeutic strategies and future research directions. Methods:A comprehensive literature review was conducted, integrating recent advances from global studies to explore macrophage-related pathways and functional alterations in UC. Special attention was given to studies investigating molecular mechanisms underlying macrophage polarization and function. Results:Evidence indicates that macrophage dysfunction is a central mechanism in the pathogenesis of UC. Major findings demonstrate that metabolic reprogramming serves as a fundamental pathway inducing phenotypic and functional alterations in macrophages. Additional mechanisms mediating these changes include epigenetic modifications, chemokine-driven recruitment, microbial metabolite induction, autophagy, and apoptosis. Multiple drugs targeting macrophages have shown effectiveness in treating UC. Conclusion:Targeting macrophage-related pathways represents an effective therapeutic approach for UC. This review provides a theoretical foundation for developing precision treatments focused on macrophage modulation and highlights important new avenues for future research.

Ulcerative colitis (UC) is an autoimmune disease with an incompletely understood pathogenesis. The Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signaling pathway plays a key role in immune response and inflammation. More and more studies demonstrated that JAK/STAT signaling pathway is associated with the pathogenesis of UC. The JAK/STAT pathway affects UC in multiple ways by regulating intestinal inflammatory response, affecting intestinal mucosal barrier, modulating T cell homeostasis, and regulating macrophages. Encouragingly, natural products are promising candidates for the treatment of UC. Natural products have the advantage of being multi-targeted and rich in therapeutic modalities. This review summarized the research progress of JAK/STAT pathway-mediated UC. Furthermore, the latest studies on natural products targeting the JAK/STAT pathway for the treatment of UC were systematically summarized, including active ingredients such as arbutin, aloe polysaccharide, berberine, matrine, curcumin, Ginsenoside Rh2, and so on. The aim of this paper is to provide new ideas for drug development to regulate JAK/STAT signaling for treating UC.

Digestive diseases remain a major challenge to public health systems globally. Cyclic GMP-AMP synthase (cGAS) and stimulator of interferon gene (STING) play important roles in innate immunity as well as inflammatory responses. Dysregulation of the cGAS-STING pathway has been demonstrated to be an important pathogenetic mechanism in diverse gastrointestinal diseases. Therefore, targeting the cGAS-STING pathway is a potential therapeutic strategy for digestive diseases. Encouragingly, increasing studies have revealed that natural plant products are promising candidates for the treatment of digestive disorders. This review discussed the research progress of cGAS-STING pathway mediating common digestive diseases, including inflammatory bowel disease, liver disease, colorectal cancer, gastric cancer, esophageal cancer, pancreatitis, and pancreatic cancer. In addition, we systematically summarized recent advances in the treatment of gastrointestinal disorders with phytochemicals that target the cGAS-STING pathway.

BackgroundCardiovascular-kidney-metabolic (CKM) syndrome represents a major health threat globally. The newly proposed dietary index for gut microbiota (DI-GM), which quantifies dietary quality associated with gut microbiota diversity, may influence the risk of CKM syndrome. Therefore, this study examined the correlation between DI-GM and the prevalence of CKM syndrome, aiming to provide insights for preventive innovation and tailored treatment methods.MethodsThis cross-sectional study included 8,400 adults aged 20 years and older from the National Health and Nutrition Examination Survey (NHANES) 2007–2018. The potential association between the DI-GM score and CKM syndrome was evaluated using univariable and multivariable weighted logistic regression models, restricted cubic spline (RCS), and subgroup analyses.ResultsThe average age of the participants was 45.5 years, with 52.0% of the participants being male. A higher DI-GM score was significantly associated with a lower prevalence of CKM syndrome (OR = 0.87, 95% CI: 0.81 to 0.92, p < 0.001). The RCS analysis further confirmed a linear relationship between DI-GM score and CKM syndrome (p for nonlinear = 0.194). Furthermore, subgroup analysis indicated that sex potentially influenced the association between DI-GM and CKM syndrome (p for interaction = 0.004), with the protective effect being more pronounced among U. S. females.ConclusionDI-GM score exhibits an inverse correlation with the risk of CKM syndrome. Optimizing dietary patterns to improve DI-GM is associated with reduced risk of CKM syndrome.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease, the incidence of which continues to rise globally, and existing therapeutic options are limited by low drug bioavailability and systemic side effects. In this study, we systematically investigated the challenges of the special gastrointestinal environment of UC patients for oral drug delivery, such as extreme pH, degradation by digestive enzymes, metabolism of intestinal flora and obstruction of the intestinal mucosal barrier, and summarized the potential of plant-derived Exosome-like Nanovesicles (PELNs) as a novel delivery system. PELNs are produced by plant cells and mainly consist of proteins, RNA, lipids and plant active molecules. Animal and cell experiments have shown that they can treat UC through the regulation of the intestinal bacterial flora, the inhibition of inflammatory pathways, and the promotion of mucosal repair, etc. On the other hand, their small particle size (30-500 nm), negative charge and lipid bilayer structure enable them to penetrate the intestinal mucus layer, tolerate extreme pH and enzymatic degradation, and adhere to intestinal epithelial cells through electrostatic interactions, thus possessing advantages such as low immunogenicity, high stability and natural targeting. Furthermore, the engineering modification of PELNs can significantly enhance targeting and therapeutic efficacy, such as surface modification or drug loading. Future research should focus on the systematic characterization, safety validation, large-scale production and multimodal combination therapy of PELNs in order to promote their clinical translation, which not only provides an efficient delivery platform for the treatment of UC, but also opens up a new pathway for the development of natural medicines.

Ulcerative colitis(UC),a chronic inflammatory bowel disease,exhibits a globally increasing incidence.Current therapeutic strategies are limited by low drug bioavailability and systemic side effects.This study systematically explored the challenges posed by the unique gastrointestinal environment in UC patients for oral drug delivery,including extreme pH conditions,degradation by digestive enzymes,metabolism mediated by intestinal flora,and obstruction from the intestinal mucosal barrier.It further highlighted the potential of Chinese herbal medicine-derived exosome-like nanovesicles(CHMELNs)as a novel drug delivery system.CHMELNs,produced by plant cells of Chinese herbal medicines,primarily consist of proteins,RNA,lipids,and bioactive phytochemicals.They demonstrate advantages such as low immunogenicity,high stability,and inherent targeting capabilities.Their small particle size(30-500 nm),negative surface charge,and lipid bilayer membrane structure enable penetration through the intestinal mucus layer,resistance to extreme pH and enzymatic degradation,and adhesion to intestinal epithelial cells via electrostatic interactions.Engineered modifications of CHMELNs,such as surface functionalization or drug loading,significantly enhance their targeting efficacy and therapeutic outcomes.Animal and cellular experiments have demonstrated that CHMELNs alleviate UC by modulating intestinal flora,suppressing inflammatory pathways,and promoting mucosal repair.Future research should focus on systematic characterization,safety validation,scalable production,and multimodal combination therapies to advance clinical translation.CHMELNs not only provide an efficient delivery platform for UC treatment but also open new avenues for the modernization of TCM and the development of natural pharmaceuticals.

Background:Mounting research suggests that insulin resistance (IR) is associated with Helicobacter pylori (H. pylori) infection. The triglyceride-glucose (TyG) index has received widespread attention due to its high sensitivity in assessing IR. This study examined the association between H. pylori infection and TyG index. Methods:This cross-sectional study used data from the National Health and Nutrition Examination Survey (NHANES) 1999 - 2000. Participants were categorized into quartile groups (Q1-Q4) based on their TyG index. Weighted multivariable-adjusted logistic regression and subgroup analysis were used to explore the correlation between TyG index and H. pylori infection. Furthermore, sensitivity analysis was conducted to assess the robustness of our findings. Results:This study included 2,918 participants, 1,101 of whom were infected with H. pylori. The mean TyG index for all participants was 8.56 ± 0.67. Patients who were H. pylori positive had higher levels of TyG index compared with H. pylori seronegative participants (8.74 ± 0.03 vs. 8.57 ± 0.03, P < 0.05). The fourth quartile of the TyG index showed the highest odds of H. pylori infection compared to Q1 (OR = 2.37, 95%CI: 1.52 to 3.71, P  <  0.001). Sensitivity analysis indicated that the association between TyG index and H. pylori infection remained strong even after excluding participants with cardiovascular diseases or taking lipid-lowering medications, as well as patients with diabetes or taking glucose-lowering medications. Conclusions:In this study, a stable and strong positive association was found between TyG index and H. pylori infection. IR may be significantly associated with H. pylori infection. Further studies are necessary to elucidate the underlying mechanisms and potential clinical implications of these findings.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease (IBD) characterized primarily by immune dysregulation. Its pathogenesis involves multiple factors, including dysregulation of T-cell subsets, hypersecretion of pro-inflammatory cytokines, imbalance in the gut microbiota, and disruption of the intestinal barrier. Among T-cell subsets, abnormal activation of Th1 and Th17 cells, in conjunction with Treg dysfunction, significantly amplifies local pro-inflammatory signals. Pro-inflammatory cytokines, such as TNF-α, IL-6, and IL-17, exacerbate apoptosis and disrupt tight junctions (TJs) in intestinal epithelial cells (IECs), thereby creating favorable conditions for invasion by pathogenic bacteria and their metabolites. Intestinal microecological imbalance not only leads to significant alterations in the structure of the bacterial flora but also involves abnormal fluctuations in its metabolites that directly regulate intestinal immune homeostasis, a factor closely associated with the severity of inflammation and prognosis of ulcerative colitis. Recent studies have demonstrated that in the treatment of UC, traditional Chinese medicine (TCM) achieves a multi-target, multi-pathway integrated intervention by regulating immune cell differentiation, balancing inflammatory factor levels, repairing the intestinal epithelial barrier, and remodeling the structure of the bacterial flora. This article reviews the pathogenic mechanisms underlying immune dysregulation in UC and the advances in research on TCM’s role in immune regulation, anti-inflammatory repair, and flora modulation, encompassing the mechanisms of action of individual active ingredients and classic TCM compound formulas. Although some studies have preliminarily confirmed TCM’s potential to modulate immunity and repair the intestinal barrier, breakthroughs in mechanism analysis, herb standardization, and large-scale validation remain forthcoming. It is anticipated that the unique advantages of TCM will be translated into a more precise therapeutic strategy for UC through modern molecular and systems biology approaches.

Objective This study evaluated the relationships between dietary magnesium and calcium intake and symptoms of chronic diarrhea and inflammatory bowel disease (IBD). Globally, the prevalence of IBD and chronic diarrheal symptoms is increasing. Research on nutritional factors in the diet associated with IBD and chronic diarrheal symptoms may be helpful. Method We performed a cross-sectional analysis utilizing the National Health and Nutrition Examination Survey (NHANES) data in 2005-2010. Information on dietary calcium and magnesium intake was assessed using the first 24-hour dietary recall interview, and IBD and chronic diarrheal symptoms were presented by questionnaire. Correlations were examined using multivariable logistic regression equations. Result After adjusting for relevant variables, those with higher dietary intakes of calcium and magnesium showed a higher frequency of IBD (highest quartile calcium intake: OR = 3.685, 95% CI = 1.572-8.641; highest quartile magnesium intake: OR = 2.985, 95% CI = 1.256-7.094), and similar results were observed in chronic diarrheal symptoms (highest quartile calcium intake: OR = 1.115, 95% CI = 1.001-1.242; third and fourth quartiles of magnesium intake: OR = 1.155, 95% CI = 1.038-1.285; OR = 1.144, 95% CI = 1.024-1.277). The inflection points for calcium and magnesium intake with chronic diarrheal symptoms were 1690 mg and 351 mg. Subgroup analyses revealed that a stronger correlation between dietary calcium and chronic diarrheal symptoms was more significant among elderly adults (≥60 years), participants with hypertension, and Mexican-American people. Conversely, the link between dietary magnesium and chronic diarrheal symptoms was stronger in females and participants with hypertension. Conclusion In conclusion, higher dietary calcium and magnesium intakes were associated with higher prevalence of IBD and chronic diarrheal symptoms, this will draw attention to daily calcium and magnesium intake in patients with IBD and chronic diarrheal symptoms.

BackgroundPrevious studies have shown conflicting results regarding the impact of circulating antioxidants on the risk of inflammatory bowel disease (IBD). In this study, our intent was to investigate the causal relationship between circulating antioxidants and IBD using Mendelian randomization (MR).MethodsInstrumental variables for absolute circulating antioxidants (ascorbate, retinol, lycopene, and β-carotene) and circulating antioxidant metabolites (α-tocopherol, γ-tocopherol, ascorbate, and retinol) were screened from published studies. We obtained outcome data from two genome-wide association study (GWAS) databases, including the international inflammatory bowel disease genetics consortium (IIBDGC, 14,927 controls and 5,956 cases for Crohn’s disease (CD), 20,464 controls and 6,968 cases for ulcerative colitis (UC), and 21,770 controls and 12,882 cases for IBD) and the FinnGen study (375,445 controls and 1,665 cases for CD, 371,530 controls and 5,034 cases for UC, and 369,652 controls and 7,625 cases for IBD). MR analysis was performed in each of the two databases and those results were pooled using meta-analysis to assess the overall effect of exposure on each phenotype. In order to confirm the strength of the findings, we additionally conducted a replication analysis using the UK Biobank.ResultsIn the meta-analysis of the IIBDGC and FinnGen, we found that each unit increase in absolute circulating level of retinol was associated with a 72% reduction in the risk of UC (OR: 0.28, 95% CI: 0.10 to 0.78, P=0.015). The UC GWAS data from the UK Biobank also confirmed this causal relationship (OR: 0.99, 95% CI: 0.97 to 1.00, P=0.016). In addition, there was suggestive evidence that absolute retinol level was negatively associated with IBD (OR: 0.41, 95% CI: 0.18 to 0.92, P=0.031). No other causal relationship was found.ConclusionOur results provide strong evidence that the absolute circulating level of retinol is associated with a reduction in the risk of UC. Further MR studies with more instrumental variables on circulating antioxidants, especially absolute circulating antioxidants, are needed to confirm our results.

Ulcerative colitis (UC) is a complex immune-mediated chronic inflammatory bowel disease. It is mainly characterized by diffuse inflammation of the colonic and rectal mucosa with barrier function impairment. Identifying new biomarkers for the development of more effective UC therapies remains a pressing task for current research. Ferroptosis is a newly identified form of regulated cell death characterized by iron-dependent lipid peroxidation. As research deepens, ferroptosis has been demonstrated to be involved in the pathological processes of numerous diseases. A growing body of evidence suggests that the pathogenesis of UC is associated with ferroptosis, and the regulation of ferroptosis provides new opportunities for UC treatment. However, the specific mechanisms by which ferroptosis participates in the development of UC remain to be more fully and thoroughly investigated. Therefore, in this review, we focus on the research advances in the mechanism of ferroptosis in recent years and describe the potential role of ferroptosis in the pathogenesis of UC. In addition, we explore the underlying role of the crosslinked pathway between ferroptosis and other mechanisms such as macrophages, neutrophils, autophagy, endoplasmic reticulum stress, and gut microbiota in UC. Finally, we also summarize the potential compounds that may act as ferroptosis inhibitors in UC in the future.

Ulcerative colitis (UC) is characterized by chronic non-recessive inflammation of the intestinal mucosa involving both innate and adaptive immune responses. Currently, new targeted therapies are urgently needed for UC, and neutrophil extracellular traps (NETs) are new therapeutic options. NETs are DNA-based networks released from neutrophils into the extracellular space after stimulation, in which a variety of granule proteins, proteolytic enzymes, antibacterial peptides, histones, and other network structures are embedded. With the deepening of the studies on NETs, their regulatory role in the development of autoimmune and autoinflammatory diseases has received extensive attention in recent years. Increasing evidence indicates that excess NETs exacerbate the inflammatory response in UC, disrupting the structure and function of the intestinal mucosal barrier and increasing the risk of thrombosis. Although NETs are usually assigned a deleterious role in promoting the pathological process of UC, they also appear to have a protective role in some models. Despite such progress, comprehensive reviews describing the therapeutic promise of NETs in UC remain limited. In this review, we discuss the latest evidence for the formation and degradation of NETs, focusing on their double-edged role in UC. Finally, the potential implications of NETs as therapeutic targets for UC will be discussed. This review aims to provide novel insights into the pathogenesis and therapeutic options for UC.

Background: The metabolites produced from choline contribute to atherosclerosis (AS) pathogenesis, and the gut microbiota is redundantly essential for this process. Indole-3-carbinol (I3C), found in cruciferous vegetables such as broccoli, cabbage, cauliflower and brussels sprouts, helps prevent hyperlipidemia, maintain the gut microbiota balance, and decrease the production of trimethylamine-N-oxide (TMAO) from choline in the diet. Purpose: The objective of this research was to investigate the impact of I3C on choline-induced AS and to further elucidate the underlying mechanism involved. Methods: AS models of high-choline-induced ApoE-/- mice and TMAO-promoted foamy macrophages were established to observe the effect of I3C on the formation of atherosclerotic plaques and foam cells and changes in AS-related indicators (including blood biochemical indicators, TMA, TMAO, SRA, and SRB1), and integrated analyses of the microbiome and metabolome were used to reveal the mechanism of action of I3C. Results: We found that I3C inhibited high-choline-induced atheroma formation (50-100 mg/kg/d, in vivo) and slightly improved the lipid profile (15 mg/kg/d, in vivo). Moreover, I3C suppressed lipid influx at a concentration of 40 mu mol/L in vitro, enhanced the diversity of the gut microbiota and the abundance of the phylum Verrucomicrobia, and consequently modified the gut microbial metabolites at a dosage of 50 mg/kg/d in the mice. Associative analyses based on microbiome and metabolomics revealed that 1-methyladenosine was a key modulator of the protective effect of I3C against AS in high-choline-induced ApoE-/- mice. Conclusion: These findings demonstrate for the first time that I3C ameliorates AS progression through remodeling of the gut microbiome and metabolomics, which paves the way for the possible therapeutic use of this vegetablederived natural compound and may reduce the clinical severity of AS-related cardiovascular diseases.

The incidence of inflammatory bowel disease (IBD) is rising worldwide, but epidemiological data on children and adolescents are lacking. Understanding the global burden of IBD among children and adolescents is essential for global standardization of methodology and treatment options. This is a cross-sectional study based on aggregated data. We estimated the prevalence and incidence of IBD in children and adolescents between 1990 and 2019 according to the Global Burden of Disease Study 2019 (GBD 2019). Age-standardized rates (ASRs) and estimated annual percentage changes (EAPCs) were used to compare the burden and trends between different regions and countries. In 2019, there were 25,659 new cases and 88,829 prevalent cases of IBD among children and adolescents globally, representing an increase of 22.8

Centrally mediated abdominal pain syndrome (CAPS) has generated a heavy disease burden worldwide. This study aimed to explore the serum exosomal microRNAs (miRNAs) as potential diagnostic biomarkers for CAPS. From September 2022 to October 2023, 97 patients with CAPS and 96 healthy subjects were enrolled. Differentially expressed serum exosomal miRNAs between patients with CAPS and healthy controls were identified by high-throughput sequencing and quantitative real-time polymerase chain reaction. The receiver operating characteristic curves and multivariate logistic regression analysis were used to evaluate the diagnostic value of the serum exosomal miRNAs. MiR-6850-5p, miR-194-5p, miR-199a-3p, and miR-4525 were significantly downregulated in serum exomes of CAPS patients compared with healthy controls, which yielded the area under curve (AUC) values of .914 (95% confidence interval (CI), .873-.954), .767 (95% CI, .695-.839), .617 (95% CI, .527-.708), and .561 (95% CI, .465-.656), respectively, to distinguish CAPS patients from healthy subjects. And AUC of the integration of the above 4 miRNAs was .931 (95% CI, .896-.966). Multivariate logistic regression indicated that hsa-miR-6850-5p (odds ratio (OR) = .046, P < .001), anxiety (OR = 7.670, P = .025), and depression (OR = 22.967, P = .008) were the independent predictors of CAPS. Serum exosomal miR-6850-5p is a promising diagnostic biomarker for CAPS. PERSPECTIVE: This study may be the first to explore serum exosomal miRNAs as new diagnostic biomarkers for CAPS, and the findings may help clinicians to access comprehensive understanding and accurate diagnosis of CAPS.

Ulcerative colitis (UC) is a chronic inflammatory bowel disease primarily affecting the mucosa of the colon and rectum. UC is characterized by recurrent episodes, often necessitating lifelong medication use, imposing a significant burden on patients. Current conventional and advanced treatments for UC have the disadvantages of insufficient efficiency, susceptibility to drug resistance, and notable adverse effects. Therefore, developing effective and safe drugs has become an urgent need. Autophagy is an intracellular degradation process that plays an important role in intestinal homeostasis. Emerging evidence suggests that aberrant autophagy is involved in the development of UC, and modulating autophagy can effectively alleviate experimental colitis. A growing number of studies have established that autophagy can interplay with endoplasmic reticulum stress, gut microbiota, apoptosis, and the NLRP3 inflammasome, all of which contribute to the pathogenesis of UC. In addition, a variety of intestinal epithelial cells, including absorptive cells, goblet cells, and Paneth cells, as well as other cell types like neutrophils, antigen-presenting cells, and stem cells in the gut, mediate the development of UC through autophagy. To date, many studies have found that natural products hold the potential to exert therapeutic effects on UC by regulating autophagy. This review focuses on the possible effects and pharmacological mechanisms of natural products to alleviate UC with autophagy as a potential target in recent years, aiming to provide a basis for new drug development.

BackgroundOxidative stress is a key contributor to the development of chronic kidney disease (CKD) in individuals with metabolic syndrome (MetS). The oxidative balance score (OBS) is an emerging composite assessment tool for dietary and lifestyle oxidative balance. We aimed to explore the association of OBS with CKD prevalence in MetS in this national cross-sectional analysis.MethodsThis was a national cross-sectional analysis. Eligible MetS participants ≥20 years of age from NHANES 1999–2018 were included. OBS was assessed according to previous well-validated methods and consisted of 16 dietary components and 4 lifestyle components. MetS was diagnosed by NCEP-ATP III criteria, while CKD was diagnosed by KDIGO 2021 Clinical Practice Guideline. Multivariate logistic regression models were used to explore the association of OBS with CKD in MetS in this national cross-sectional analysis.ResultsA total of 8,095 MetS participants were included, with a CKD prevalence of 24.8%. In fully adjusted models, each score increases in OBS, dietary OBS, and lifestyle OBS was associated with a 2, 1.7, and 7.3% reduction in the prevalence of CKD, respectively. Higher OBS, dietary OBS, and lifestyle OBS were all associated with significantly lower odds of CKD (p for trend all <0.05). Restricted cubic spline analysis showed that these associations all exhibited inverse dose–response. Interaction analyses indicated that cardiovascular disease (CVD) status significantly influenced the impact of OBS and dietary OBS, and these associations were only present in CVD-free subjects. Defining MetS using the IDF criteria did not significantly change the results.ConclusionOBS was inversely associated with the prevalence of CKD in MetS, especially in CVD-free settings. These findings emphasize that adherence to an antioxidant diet and lifestyle contributes to the early prevention of CKD in the MetS population and necessitates attention to CVD interactions. Future prospective cohort studies are needed to confirm these results.