Micro- and nanoplastics (MNPs) are pervasive environmental contaminants with growing recognition as potential contributors to human disease. Widespread human exposure occurs primarily through ingestion of contaminated food and water, and MNPs have been detected in multiple human tissues, including the gastrointestinal tract. Experimental evidence provides a plausible biological basis for disease associations, including impairment of intestinal barrier integrity, activation of mucosal immune pathways, and alteration of gut microbial communities caused by MNP exposure. Although human data remain limited, early studies demonstrate MNP detection in stool and suggest potential correlations with inflammatory biomarkers such as fecal calprotectin. These findings, together with mechanistic data from in vitro and animal models, raise concern that MNP exposure represents a paradigm shift in the pathogenesis or modulation of inflammatory bowel disease (IBD); however, methodological variability, small sample sizes, and contamination challenges currently limit definitive conclusions. The aim of this review is to evaluate the current understanding of MNP exposure and its impact on intestinal health, particularly in relation to IBD. We synthesize mechanistic and early clinical evidence linking MNPs to IBD and highlight critical research gaps. Future standardized exposure assessment, mechanistic validation in human systems, and longitudinal studies are essential to clarify causal relationships. Given the modifiable nature of environmental plastic exposure, advancing this field may offer new opportunities for IBD prevention and intervention.

Cirrhotic cardiomyopathy (CCM) is a significant complication of cirrhosis, but its progression and underlying mechanisms remain incompletely understood. This study aimed to investigate dynamic changes in cardiac function, pathology, inflammation, and mitochondrial damage in a mouse model of CCM, and to compare echocardiographic characteristics in patients with cirrhosis.

Bile duct ligation was performed in male C57BL/6J mice to induce cirrhosis. Longitudinal analyses were conducted over eight weeks. Cardiac function was assessed using serum biomarkers, echocardiography, and electrocardiography. Pathology was examined with hematoxylin and eosin, Masson’s trichrome, Sirius Red, and wheat germ agglutinin staining. Western blotting and immunohistochemistry were used to detect markers of inflammation, fibrosis, apoptosis, and mitochondrial function. Cardiac and liver function markers were also evaluated in patients with cirrhosis.

Mice subjected to bile duct ligation developed progressive cardiac dysfunction, including reduced cardiac output and diastolic dysfunction (end-diastolic interventricular septal thickness, left ventricular internal diameters, stroke volume, and left ventricular end-diastolic volume decreased, whereas ejection fraction and fractional shortening increased), as well as cardiac atrophy. Myocardial apoptosis, inflammation (elevated tumor necrosis factor, interleukin-6, and p65), and fibrosis worsened over time. Mitochondrial injury was characterized by reduced carnitine palmitoyltransferase 1A and peroxisome proliferator-activated receptor alpha, with increased hexokinase 2, pyruvate kinase M2, and lactate dehydrogenase A. In patients with cirrhosis, impaired cardiac function and elevated brain natriuretic peptide levels correlated with total bilirubin.

The progression of CCM is closely associated with cirrhosis severity and appears to be driven by myocardial atrophy, apoptosis, inflammation, fibrosis, and mitochondrial dysfunction.

Infections are frequent and lethal complications of acute-on-chronic liver failure (ACLF). Reliable biomarkers to distinguish fungal from bacterial infections remain limited. Given the central role of immune dysfunction in ACLF, we aimed to evaluate the diagnostic value of serum cytokines in differentiating invasive pulmonary aspergillosis (IPA) from bacterial pneumonia (BP) in HBV-associated ACLF.

This retrospective case-control study enrolled ACLF patients admitted to the Tongji Hospital, between 2018 and 2022. Patients were categorized into IPA, BP, and non-infection groups. The BP and non-infection groups were propensity score-matched to the IPA cases. Serum cytokines levels (IL-1β, sIL-2R, IL-6, IL-8, IL-10, TNF-α) and clinical data were collected, with the diagnostic performance of these cytokines as biomarkers assessed via ROC curves.

A total of 32 IPA, 96 BP, and 96 non-infection patients were enrolled, with balanced baseline characteristics. Compared with the non-infection group, the IPA group had higher sIL-2R (1,606.00 vs. 1,211.50 U/mL, P = 0.019) and IL-6 (69.03 vs. 15.98 pg/mL, P < 0.001) levels, but lower IL-8 levels (62.20 vs. 132.00 pg/mL, P = 0.025). The BP group showed elevated sIL-2R (1,792.00 U/mL), IL-6 (49.42 pg/mL), IL-10 (13.40 pg/mL) levels compared to the non-infection group (all P < 0.001). Also, IL-8 was lower in the IPA group than in the BP group (62.20 vs. 176.00 pg/mL, P < 0.001) and its assessment could best distinguish IPA from BP (AUC = 0.743, cut-off = 76.60 pg/mL; sensitivity = 66.7%, specificity = 82.1%).

Serum IL-8 exhibited superior diagnostic value for IPA in patients with HBV-ACLF and could effectively discriminate Aspergillus infections from bacterial infections.

Diabetic cardiomyopathy (DCM), a diabetes-specific cardiovascular complication, is pathologically characterized by cardiomyocyte apoptosis, oxidative stress, inflammatory responses, and myocardial fibrosis, distinguishing it from other cardiac disorders, such as hypertension and coronary artery disease. Challenges in early diagnosis, coupled with the limited efficacy and adverse effects of current treatments, have made DCM a significant contributor to heart failure and mortality in patients with diabetes. Natural products, recognized for their diverse sources, structural variety, and multitarget therapeutic potential, have shown promise in preventing and treating DCM. Drawing on advances over the past five years, this review systematically summarizes the pharmacological effects and molecular mechanisms of natural products (e.g., flavonoids, terpenoids, phenylpropanoids, alkaloids, and polysaccharides) in the treatment of DCM, with the aim of providing a theoretical foundation for further research and drug development.

PVT is a harmful event in cirrhosis, and the prevention and treatment of PVT are important in the management of cirrhosis and portal hypertension. The study aimed to observe the efficacy of Danggui Buxue Decoction (DBD) on portal vein thrombosis (PVT) in cirrhosis and to elucidate the related mechanism using a modified animal model.

A model of PVT in cirrhosis was established by partial portal vein ligation and intraperitoneal injection of CCl4 in rats, which showed obvious PVT with intra- and extravenous thrombosis as well as liver cirrhosis. Rats were randomly assigned into four groups and received intragastric administration of DBD (12 g/kg/day) or rivaroxaban (20 mg/kg/day) for 6 weeks.

DBD attenuated collagen deposition and reduced thrombus formation in model livers, increased portal vein blood flow, expanded the portal vein diameter, and reduced prothrombin time and international normalized ratio in the model rats. In addition, DBD reduced hepatic von Willebrand factor and plasminogen activator inhibitor-1 expression and increased hepatic fibrin degradation product content in the liver tissues of model rats.

We modified a model of cirrhotic PVT in rats and found that DBD had a good effect on PVT and liver fibrosis, with the mechanisms related to the enhancement of portal vein blood flow and the protection against endothelial cell injury.

5-methylcytosine RNA modification is a key regulator of neuroblastoma oncogenesis and differentiation. NSUN6, a 5-methylcytosine-specific messenger RNA methyltransferase, modulates messenger RNA methyltransferase activity and translation termination. Yet, its potential link to neuroblastoma risk has not been previously reported. The present study aimed to reveal the relationship between NSUN6 gene polymorphisms and the risk of neuroblastoma in children from Jiangsu province.

In this case-control study, we investigated three NSUN6 gene polymorphisms (rs3740102 A>C, rs12780826 T>A, and rs61842187 G>C) in 402 neuroblastoma cases and 473 controls, all of whom were children from Nanjing City, Jiangsu Province, China. DNA from these subjects was assessed using the TaqMan method. Multivariate logistic regression analysis was employed to examine the association between NSUN6 gene polymorphisms and neuroblastoma risk. Additionally, the Genotype-Tissue Expression database was utilized to elucidate the impact of these polymorphisms on NSUN6 and nearby gene expression. Kaplan-Meier analysis and the non-parametric test were conducted on the R2 platform to assess the relationship between gene expression, prognosis, and neuroblastoma risk.

Carriage of two to three protective genotypes (rs3740102 AA/AC, rs12780826 TT/TA, rs61842187 CC) was significantly associated with a lower risk of neuroblastoma (adjusted odds ratio = 0.41, 95% confidence interval = 0.23–0.73, P = 0.002), with consistent results across all subgroups. Expression quantitative trait locus analysis showed these single-nucleotide polymorphisms may upregulate the expression of NSUN6 and CACNB2. Furthermore, higher NSUN6 and CACNB2 expression was correlated with a potentially lower risk of neuroblastoma, improved overall survival (NSUN6: P = 2.54e-03; CACNB2: P = 6.35e-06) and event-free survival (NSUN6: P = 7.90e-04; CACNB2: P = 4.64e-06), as well as a lower likelihood of MYCN amplification.

NSUN6 rs3740102 AA/AC, rs12780826 TT/TA, and rs61842187 CC genotypes may be associated with a better prognosis of neuroblastoma. This association may be related to the potential upregulation of NSUN6 gene expression and a lower likelihood of MYCN amplification.