Pancreatic fibrosis, a major pathological feature of chronic pancreatitis, is primarily driven by the abnormal activation of pancreatic stellate cells (PSCs) and excessive deposition of extracellular matrix. Traditional Chinese medicine (TCM) offers a holistic and synergistic approach to preventing and treating pancreatic fibrosis through multi-target regulation of PSC activation. This review systematically elucidates the mechanisms by which TCM—encompassing both bioactive monomers and compound formulations—modulates key signaling pathways involved in PSC activation, including the mitogen-activated protein kinase, transforming growth factor-β/Smad, platelet-derived growth factor, nuclear factor kappa B, and Wingless/β-catenin pathways. By simultaneously targeting these interconnected signaling networks, TCM strategies effectively inhibit PSC activation, attenuate inflammatory responses, and reduce extracellular matrix deposition. In contrast to single-target pharmacological inhibitors, TCM embodies a “multi-component, multi-pathway” therapeutic paradigm that aligns with the complex pathophysiology of pancreatic fibrosis. This review also draws comparative insights from liver fibrosis, highlighting conserved pathways and organ-specific regulatory contexts. Ultimately, TCM represents a promising integrative avenue for the prevention and treatment of pancreatic fibrosis, supported by growing preclinical evidence and aligned with the principles of holistic intervention.

Hepatocellular carcinoma (HCC) is one of the most prevalent and aggressive malignant tumors globally, with a notably low five-year survival rate. Its high mortality is largely attributed to challenges in early detection. Extracellular vesicles (EVs) are naturally occurring nanoparticles secreted by nearly all cell types and carry a diverse array of bioactive molecules, including proteins, nucleic acids (particularly non-coding RNAs), and lipids. EVs play pivotal roles in remodeling the tumor microenvironment and driving cancer progression through intercellular communication. Accumulating evidence has established that EVs are critically involved in the pathogenesis of HCC and are emerging as promising biomarkers for its early detection. With advances in EV isolation technologies, these vesicles have garnered considerable attention in the field of liquid biopsy for HCC. This review provides a comprehensive overview of the diagnostic potential of EV-derived biomarkers in HCC, including DNA, RNA, proteins, and lipids. Additionally, it discusses the advantages of integrating multi-omics approaches for HCC diagnosis. Furthermore, the review highlights the technical challenges in EV isolation and characterization, as well as the crucial role of reference genes in the standardization of EV data. These insights underscore the potential of EVs as novel, minimally invasive liquid biopsy biomarkers for the early diagnosis of HCC.

Pancreatic cancer remains a highly lethal malignancy owing to the difficulty of early detection. In 2021, the Chinese Consensus on Early Screening and Surveillance for Pancreatic Cancer in High-risk Individuals was first established. However, the evidence landscape has evolved rapidly, necessitating an updated, evidence-based framework tailored to the Chinese healthcare context. This revised consensus aims to standardize the early screening and surveillance process for high-risk populations in China. A multidisciplinary expert panel comprising 53 specialists from 17 provincial-level regions systematically reviewed the literature using the GRADE (Grading of Recommendations Assessment, Development and Evaluation) methodology. A modified Delphi process was employed, with consensus predefined as ≥75% agreement. The panel formulated 26 evidence-based recommendations covering screening objectives, the definition of high-risk populations (hereditary susceptibility, new-onset diabetes, chronic pancreatitis, and pancreatic cystic neoplasms), age at screening initiation, surveillance intervals, imaging modalities (magnetic resonance imaging/magnetic resonance cholangiopancreatography, endoscopic ultrasound, computed tomography), surgical indications, and lifestyle modifications. Of these recommendations, 14 are strong and 12 are weak, supported by evidence levels ranging from A to D. Implementation of this consensus in clinical practice will help improve the early diagnosis of stage I pancreatic cancer and high-grade precursor lesions, thereby advancing standardized multidisciplinary care and ultimately improving patient outcomes in China.

Insulin resistance is a common extrahepatic manifestation of hepatitis C virus (HCV) infection (HCVi), but its mechanism is poorly understood. While systemic insulin resistance is documented, portal insulin dynamics, a key regulator of hepatic metabolism, remain unexplored. This study aimed to investigate the relationship between insulin, the gut-liver axis, and immunometabolic changes in patients with HCV.

HCV patients were evaluated before (HCVi; n = 29) and after sustained virologic response (SVR) achieved with sofosbuvir/velpatasvir treatment (SVR, n = 23) (NCT02400216). Liver biopsies, portal blood, and peripheral blood were collected at both phases. Statistical analyses were conducted using Wilcoxon rank-sum tests, Mann-Whitney tests, and Pearson’s correlation coefficients to assess differences and associations across insulin, glucose, cytokines, metabolites, immune cells, and hepatic liver transcriptomics to elucidate impaired insulin homeostasis in HCVi.

HCV patients had significantly reduced portal insulin compared to SVR (p = 0.02), while peripheral insulin, portal glucose, and peripheral glucose remained unchanged. Portal insulin correlated positively with proinflammatory cytokines and vascular injury markers and negatively with CD8/CD62L/CD45RA/CD3 cells (naive cytotoxic T-cells) and non-standard nucleotides. Hepatic transcriptomic analysis revealed portal insulin correlated positively with immune and negatively with amino acid pathways, reflecting insulin’s role in the perturbations of immunometabolism during HCVi.

Lower portal insulin during HCVi is associated with changes consistent with altered pancreatic insulin secretion and decreased hepatic insulin extraction. The observed correlations support a potential relationship between the immune response and insulin dynamics, indicating an interplay between the immune system, metabolism, and insulin in HCVi, with clinical implications for the management of dysglycemia.

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.

Comparative data on sequential transarterial chemoembolization (TACE) after stereotactic body radiation therapy (SBRT) in recurrent hepatocellular carcinoma (HCC) remain limited. This study aimed to evaluate the efficacy of this combination.

We retrospectively reviewed 152 patients with recurrent HCC who met predefined eligibility criteria; 109 received SBRT alone and 43 received SBRT plus TACE. To minimize selection bias, a 2:1 propensity score matching was performed, resulting in 68 patients in the SBRT-alone group and 36 in the SBRT plus TACE group for the final comparative analysis. Overall survival, progression-free survival, and local control were assessed using the Kaplan-Meier method.

The SBRT plus TACE group was associated with numerically higher survival rates, although this difference did not reach statistical significance. The cumulative one-, three-, and five-year overall survival rates were 91.2%, 76.3%, and 61.8% for SBRT alone, compared to 100.0%, 86.1%, and 77.5% for the combination therapy ( p = 0.069). The corresponding progression-free survival rates were 73.1%, 51.1%, and 32.3% versus 88.9%, 58.1%, and 52.3% ( p = 0.091). No acute grade ≥3 toxicities were observed in either group.

In this exploratory analysis of recurrent HCC, the combination of SBRT and TACE demonstrated a favorable trend toward improved survival compared with SBRT alone, without an increase in severe toxicity. While these findings did not reach statistical significance, they establish the safety profile of the combined approach and provide preliminary evidence supporting its potential therapeutic role. This hypothesis-generating study justifies and informs the design of larger, prospective trials to definitively evaluate the efficacy of this regimen.

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.

Chikungunya fever, caused by the Chikungunya virus (CHIKV), has re-emerged as a significant global health concern in recent decades. A notable event was the largest-ever local outbreak in China in 2025, marking a critical juncture in its epidemiology. Although conventional treatment remains predominantly supportive, the integration of traditional Chinese medicine (TCM) offers promising complementary strategies for alleviating both acute symptoms and chronic polyarthralgia. This narrative review aims to consolidate current knowledge on the etiology, pathogenesis, clinical manifestations, and management of Chikungunya fever, with a particular focus on the evidence-based application of TCM. By integrating molecular virology with clinical and epidemiological insights, this review offers a comprehensive perspective on the challenges posed by CHIKV and underscores the strategic imperatives essential for its future management. In conclusion, addressing the expanding threat of CHIKV necessitates a multi-pronged public health strategy that integrates standard clinical and preventive measures with evidence-based TCM therapies, highlighting the urgent need for rigorous clinical trials to globally validate these integrative treatments.

Breast cancer (BCA) is one of the most common cancers worldwide, with a high rate of mortality and morbidity in women. This review focuses on the applications of nanotechnology, nanomaterials, and nanoparticles (NPs) in BCA, encompassing diagnosis and therapy. Nanotechnologies, nanocarriers, and nano-encapsulations versus their corresponding counterparts for BCA diagnosis and therapy have been discussed. Various drug formulations into different nanocarriers (lipid NPs, nanoemulsions, polymeric NPs, and metal-based NPs) enhanced their bioavailability and therapeutic efficacy, overcoming the limitations of conventional formulations. Additionally, clinical specialists have achieved improved outcomes in the detection and monitoring of BCA at various stages using nanotechnology, ultimately leading to an improved quality of life for patients.

N6-methyladenosine (m6A), the most prevalent internal RNA modification in eukaryotic cells, is a dynamic regulator of RNA metabolism and cancer biology. In colorectal cancer (CRC), dysregulated m6A reshapes transcriptomic programs that control tumor growth, metastasis, immune evasion, and therapeutic resistance. However, the context-dependent functions of individual m6A regulators remain incompletely defined, the integration of m6A with canonical oncogenic signaling remains incomplete, and its role in metabolic reprogramming lacks a systematic overview. This review aims to integrate current evidence on m6A regulatory machinery in CRC, clarify its coordination with oncogenic signaling and metabolic pathways, and highlight emerging translational implications. The key players regulating m6A in CRC progression are m6A “writers”, including methyltransferase-like 3 and methyltransferase-like 14; m6A “erasers”, including fat mass and obesity-associated protein and AlkB homolog 5; and m6A “readers”, including the YTH m6A RNA-binding protein family and the insulin-like growth factor 2 mRNA-binding protein family. m6A modification coordinates key oncogenic pathways, including Wnt/β-catenin, PI3K/Akt, MAPK, and p53 signaling. Moreover, m6A-dependent regulation of metabolic enzymes such as hexokinase 2, pyruvate kinase M2, and fatty acid synthase promotes the reprogramming of glucose, amino acid, and lipid metabolism, linking epitranscriptomic control to bioenergetic adaptation. We also discuss context-dependent and paradoxical functions of m6A regulators and advances in m6A-targeted therapies. In conclusion, m6A modification functions as a central regulatory hub in CRC by integrating signaling networks and metabolic pathways. Deeper mechanistic insights into spatiotemporal m6A regulation may accelerate the development of biomarkers and targeted therapies for precision CRC management.