Metabolic dysfunction-associated steatotic liver disease (MASLD) is an independent risk factor for cardiovascular disease (CVD). While gut bacteria have been linked to CVD, the role of intestinal fungi in subclinical coronary atherosclerosis (SCA) remains unclear. In this study, we aimed to investigate the association between the gut mycobiome and SCA in MASLD.

A cross-sectional study was conducted among 103 MASLD patients without established CVD. Fibrosis and steatosis were assessed using magnetic resonance elastography (MRE) and proton density fat fraction, respectively. SCA was defined by coronary artery calcification (CAC). Fecal fungal composition was analyzed via internal transcribed spacer sequencing.

Mean age was 60.8 ± 11.2 years; 51.5% were men; 20.4% had cirrhosis. CAC correlated with MRE (r = 0.489, p < 0.001), interleukin-6 (r = 0.407, p < 0.001), and tumor necrosis factor-α (r = 0.254, p = 0.018), but not proton density fat fraction. Cirrhosis patients had higher CAC than F0–F3 (456.9 vs. 205.9, p = 0.033). Candida albicans (C. albicans) abundance was greater in cirrhosis and correlated with CAC (r = 0.403, p < 0.001) and MRE (r = 0.212, p = 0.032). In multivariate analysis, older age, diabetes, obesity, cirrhosis, and enriched C. albicans independently predicted CAC ≥ 100 AU in MASLD.

In MASLD, cirrhosis and C. albicans enrichment are independently associated with higher SCA burden, suggesting advanced liver disease and a potential fungal contribution to CVD pathogenesis.

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.

Invasive pituitary adenomas with infrasellar extension can present with symptoms such as epistaxis and nasal obstruction, closely mimicking the clinical and radiological characteristics of nasopharyngeal carcinoma, which frequently leads to misdiagnosis. This report discusses the case of a 32-year-old male who was initially misdiagnosed with nasopharyngeal carcinoma for approximately one month and subsequently underwent radiotherapy and chemotherapy. However, a multidisciplinary assessment at our institution, incorporating magnetic resonance imaging findings of an invasive sellar mass, serum prolactin levels exceeding 2,000 ng/mL, and positive immunohistochemistry for PIT-1 and prolactin, established the diagnosis of an invasive prolactinoma. Treatment with bromocriptine led to significant tumor reduction. However, this was complicated by cerebrospinal fluid leakage, which subsequently resulted in an intracranial infection. The patient underwent surgical resection of the tumor and repair of the cerebrospinal fluid leak, with postoperative pathology confirming a PIT1-lineage, densely granulated, prolactin-secreting adenoma. The patient experienced a favorable recovery, with prolactin levels normalizing under continued bromocriptine therapy. This case highlights the critical importance of routine hormonal screening, thorough evaluation of nasopharyngeal mucosal integrity, and multidisciplinary collaboration in the diagnostic process.

Liver transplant rejection significantly affects patient prognosis. Myeloid-derived suppressor cells (MDSCs), known for their potent immunoregulatory functions, represent a promising target for managing liver transplant rejection. This study aimed to systematically characterize the diversity of MDSC subsets and their context-dependent functions, particularly within the context of transplant tolerance.

We analyzed clinical and murine liver transplants using single-cell RNA sequencing, bulk RNA sequencing, flow cytometry, multiplex immunohistochemistry, and co-culture assays to phenotype MDSC subsets.

Single-cell RNA sequencing analysis of human and murine samples revealed MDSC involvement in transplant rejection. In mice, MDSC scores followed a normal distribution during the first week post-transplant and correlated with clinical flow cytometry data at one month. A distinct LDLR+ monocytic MDSC (M-MDSC) subset was identified and confirmed through spatial mapping by multiplex immunohistochemistry. Flow cytometry demonstrated dynamic changes in LDLR+ M-MDSCs across tissues (liver, spleen, peripheral blood, bone marrow, and lymph nodes), with a peak during acute rejection. Co-culture experiments showed that LDLR−/− M-MDSCs exhibited reduced Arg-1/iNOS expression and an impaired capacity to induce inhibitory receptors (TIGIT, PD1, CTLA-4) or suppress effector molecules (GZMB, IFN-γ, IL-2) in CD8+ T cells.

These findings highlight the critical role of MDSCs in liver transplant rejection. LDLR+ M-MDSCs exhibited enhanced immunosuppressive properties, underscoring their potential clinical relevance in mitigating rejection and promoting immune tolerance.

Chronic pancreatitis is an inflammatory disease and is difficult to manage despite advancements in medical science. This study examined the effect of water/ethanol extracts of Justicia carnea leaves on oxidative stress and glucagon expression in a mouse model of chronic pancreatitis induced by trinitrobenzenesulfonic acid (TNBS).

Twenty-five male Swiss albino mice were randomized and treated intrarectally with vehicle (the control group) or TNBS. Some TNBS-treated mice were treated orally with 200 mg/kg or 400 mg/kg J. carnea extracts, or with the positive control, 500 mg/kg sulfasalazine, every other day on three occasions. Oxidative stress markers and pancreatic glucagon expression were assessed.

Compared with the healthy control mice, treatment with TNBS significantly decreased the levels of pancreatic glutathione (0.89 µmol/g tissue vs. 7.16 µmol/g tissue in the control) and glutathione peroxidase activity, but significantly increased the levels of α-amylase and lipase activities, lipid peroxidation, total antioxidant capacity, and nitric oxide, as well as serum C-reactive protein (P < 0.05 for all), accompanied by severe inflammation and reduced glucagon expression in the pancreatic tissues. The toxic effects of TNBS were significantly mitigated by treatment with J. carnea extracts.

These findings provide evidence that treatment with J. carnea extracts inhibited oxidative stress and preserved glucagon expression in the pancreatic tissues of mice.

The nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) family regulates fundamental processes in both innate and adaptive immunity. Aberrant NF-κB activation, whether through canonical or non-canonical signaling pathways, contributes to chronic inflammation, autoimmunity, allergy, and primary immunodeficiency/autoinflammatory syndromes, while also influencing host defense and tissue repair mechanisms. The present review aims to synthesize molecular architecture, upstream triggers, ubiquitin-centered relay systems, and the dynamic regulation of NF-κB activity. The major findings on the NF-κB signaling pathway encompass its dual molecular mechanisms (canonical and non-canonical), its central roles in immune and inflammatory responses, cell survival, and development, as well as its complex regulatory networks. We interpret NF-κB as a master integrator of diverse signals, essential for both acute and long-term physiological processes. Dysregulation of NF-κB underlies many diseases, and while it is a promising therapeutic target, its ubiquitous functions demand precise modulation to avoid adverse effects. In conclusion, the proper function of the NF-κB signaling pathway is essential for maintaining cellular homeostasis and immune defense; its dysregulation is linked to chronic inflammatory diseases, autoimmune disorders, and cancer, which underscores the pathway’s significance as a therapeutic target. Although it elucidates molecular processes and treatment options, experimental validation of emerging therapeutic concepts such as ubiquitin code editing and spatial immunology remains limited.

Despite the emergence of new approaches in acute myeloid leukemia (AML) treatment in recent years, the overall prognosis remains poor. Particularly for elderly patients and relapsed/refractory cases, the five-year survival rate consistently remains below 30%. While traditional chemotherapy regimens can rapidly suppress tumor burden and alleviate clinical symptoms, they suffer from limitations such as insufficient targeting, prominent toxic side effects, and a tendency to induce drug resistance. Immunotherapy offers a novel therapeutic pathway for AML due to its advantages of precise targeting, long-lasting antitumor effects, and a controllable safety profile. However, single-agent immunotherapy demonstrates limited clinical response rates in AML and struggles to achieve complete tumor cell clearance. In this context, combination regimens of chemotherapy and immunotherapy are increasingly becoming the focus of research. This review aims to summarize the rationale and advances in the combination of immune checkpoint inhibitors, chimeric antigen receptor T-cell therapy, antibody-drug conjugates, bispecific antibodies, and cancer vaccines with chemotherapy for the treatment of AML. We have detailed the preclinical research and clinical trial progress of each combined regimen, analyzed the core challenges—including off-target toxicity, high tumor heterogeneity, and limited efficacy in specific AML subtypes—and further propose targeted solutions and future development directions, such as exploring novel specific antigens, developing multi-targeted drugs, and formulating precision individualized treatment plans. The clinical application of such combined strategies is attracting increasing attention. In conclusion, chemo-immunotherapy combinations represent a highly promising therapeutic paradigm for AML, harnessing the synergy of chemotherapy-mediated immune microenvironment remodeling and the specific antitumor activity of immunotherapies to overcome single-agent limitations and deliver meaningful survival benefits.

Hepatocellular carcinoma (HCC) is a malignant tumor with high incidence and mortality rates worldwide, in which immune evasion mechanisms play a crucial role in its progression and treatment. Natural killer group 2D ligands (NKG2DL), as key molecules activating immune cells, significantly influence the immune evasion of liver cancer through their regulatory mechanisms. This review summarizes the regulatory mechanisms of NKG2DL expression, including genetic, signaling pathway, non-coding RNA, and stress response modulation, and discusses their expression patterns and clinical relevance in HCC. Studies have shown that the expression status of NKG2DL not only impacts patient prognosis and therapeutic response but also provides potential targets for HCC immunotherapy. Future research should focus on the molecular networks regulating their expression and their synergy with immunotherapy to provide a theoretical basis for developing more precise diagnostic and personalized treatment strategies for HCC.