Metabolic dysfunction-associated steatotic liver disease (MASLD) is now the most common chronic liver disease in the Western world, driven by obesity, insulin resistance, and systemic inflammation. Its progressive form, metabolic dysfunction-associated steatohepatitis (MASH), can culminate in cirrhosis and hepatocellular carcinoma (HCC). While lifestyle modification remains central to MASLD management, there is growing interest in pharmacological interventions, particularly nutrient-stimulated hormone-based therapies (NuSHs), such as GLP-1 receptor agonists. NuSHs exert metabolic and anti-inflammatory effects primarily via weight loss and improved insulin sensitivity. Emerging clinical data support their efficacy in resolving MASH without worsening fibrosis. However, benefits in cirrhotic patients are less evident, suggesting greater utility in early intervention. Observational studies and clinical trials suggest a reduction in liver-related morbidity with GLP-1 receptor agonist use, though fibrosis regression remains inconsistent. Preclinical models indicate that NuSHs may also reduce MASH-related HCC incidence and tumor burden, likely through systemic metabolic improvements rather than direct antineoplastic action. Observational human data following bariatric surgery reinforce this link, suggesting that weight loss itself plays a key preventive role. Herein, we propose that NuSHs are promising candidates for MASH-related HCC prevention. We provide mechanistic suggestions for how this may occur. Furthermore, incorporating NuSHs into the post-locoregional treatment pathway for HCC may delay the need for systemic anti-cancer therapies, improve immunotherapy synergy and transplant eligibility, and even slow disease progression through reversal of carcinogenic drivers. Future studies are needed to target oncological endpoints and clarify immunometabolic mechanisms to guide the integration of NuSHs into MASLD treatment algorithms.

Reporting quality in clinical research is critical for evidence-based medicine and reproducibility of clinical studies. Previous work has mostly focused on the reporting quality of clinical trials and observational longitudinal studies. However, few studies have examined the reporting quality of trend analyses. Moreover, the reporting of recommended statistical metrics in trend analyses remains largely unclear. Therefore, we assessed the reporting quality of trend analyses based on reporting of recommended statistical metrics. We systematically searched the PubMed for the trend-analysis articles published in 10 leading medicine and oncology journals over an 11-year period (2008–2018). Studies published after 2019 were excluded due to a sudden, significant increase in publication numbers during and immediately after the COVID-19 pandemic. Only original articles, research letters, and meta-analyses/systematic reviews were included. We scored the reporting quality of these articles based on whether they reported p-values, effect sizes, beta/coefficient/slope/annual-percentage-change (APC). 297 articles met the inclusion criteria. Among these, 193 (66.0%) reported p-values and 216 (72.7%) reported effect sizes. Only 13 (5.8%) analyses reported neither p-values/effect sizes nor beta/coefficient/slope/APC. In multivariable regression models, authors affiliated with epidemiology departments were less likely to report effect sizes, whereas those from statistics departments were more likely to do so. Interestingly, U.S.-based senior authors (versus non-U.S.) more likely reported p-values. No factors were independently associated with reporting APC. Overall, the reporting quality of trend analyses in leading medicine and oncology journals appears moderate and warrants improvement. We thus call for increased awareness and further research on reporting quality in trend analyses in oncology research and beyond.

COVID-19 has resulted in significant long-term sequelae in convalescent patients, impacting overall quality of life. Traditional Chinese medicine (TCM) has shown promise in managing post-COVID-19 symptoms through syndrome differentiation. This study aimed to evaluate the efficacy and safety of TCM in COVID-19 convalescent patients in a real-world setting.

This prospective, real-world study will be conducted at Guangdong Provincial Hospital of Traditional Chinese Medicine. A total of 528 COVID-19 convalescent patients will be recruited and divided into two groups: a control group receiving routine Western medical treatment and an intervention group receiving additional TCM treatment based on syndrome differentiation. Patients will be assessed for three major TCM syndromes: Lung-Spleen Qi Deficiency, Qi-Yin Deficiency, and Cold Phlegm Obstructing the Lung, with corresponding TCM prescriptions administered accordingly. The primary outcome measure will be the improvement in clinical symptom scores based on a TCM symptom scoring system. Secondary outcomes will include changes in laboratory tests, imaging studies, heart function classification, and quality of life scores. Safety will be assessed through liver and kidney function tests and adverse event monitoring.

The study is expected to demonstrate that TCM treatment, based on syndrome differentiation, can significantly improve clinical symptoms and overall health in COVID-19 convalescent patients compared to routine Western medical treatment. These findings will provide evidence for integrating TCM into post-acute COVID-19 care.

This study will contribute to the evidence supporting TCM as an effective treatment for post-COVID-19 syndrome, enhancing patient outcomes and informing comprehensive recovery strategies.

Sterol regulatory element-binding protein 1 (SREBP1), a key regulator of lipogenesis, is highly expressed in tumors, but the mechanisms sustaining its elevated levels remain unclear. The role of UFMylation, a posttranslational modification, in modulating SREBP1 stability and tumor progression has not been explored. This study aimed to investigate the role of UFMylation in the progression of liver cancer.

Liquid chromatography-tandem mass spectrometry was employed to investigate the interacting proteins of ubiquitin-fold modifier 1-specific ligase 1 (UFL1). Knockdown of UFL1 and DDRGK domain-containing protein 1 (DDRGK1) was performed to assess SREBP1 stability. In vitro and in vivo models of hepatocellular carcinoma (HCC) were used to evaluate tumor progression. Clinical correlations between UFL1/DDRGK1 and SREBP1 levels were analyzed in HCC patient samples.

SREBP1 undergoes UFMylation, which synergizes with ubiquitination to reduce its stability. Depletion of UFL1 or DDRGK1 increased SREBP1 stability, driving HCC progression. Clinically, UFL1 and DDRGK1 levels were reduced in HCC tissues and inversely correlated with SREBP1 expression. Fatostatin (an SREBP1 inhibitor) enhanced the therapeutic effect of Lenvatinib in HCC models with low UFL1 expression.

UFMylation is a critical posttranslational modification that destabilizes SREBP1, and its dysregulation contributes to HCC progression. Targeting the UFMylation-SREBP1 axis, particularly through Fatostatin and Lenvatinib combination therapy, represents a novel therapeutic strategy for HCC.

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.

Bacterial infections (BIs) are common and severe complications in patients with liver cirrhosis, but global data are limited. Here, we aimed to evaluate the global prevalence, temporal changes, and associated mortality risk of BIs in liver cirrhosis.

We systematically searched PubMed, Embase, Web of Science, and the Cochrane Library for eligible studies published without language restrictions until 11 August 2025. A random-effects model was used for meta-analyses, meta-regression by study year, and pooling adjusted hazard ratios.

Fifty-nine studies, including 1,191,421 patients with cirrhosis, were analyzed. The pooled prevalence of BIs (33 studies) was 35.1% (95% confidence interval (CI): 29.2–41.4). The prevalence of Escherichia coli and Streptococcus spp. was 3.8% (95% CI: 2.5–5.2) and 1.5% (95% CI: 0.8–2.6), respectively. The pooled prevalence of multidrug-resistant bacteria was 6.8% (95% CI: 4.0–11.3). The most common BI sites were the gastrointestinal tract, ascites fluid, and urinary tract. The highest prevalence of BIs was reported in Europe (38.2%; 95% CI: 24.8–53.6), followed by South America (37.5%; 95% CI: 29.7–46.1) and Asia (22.8%; 95% CI: 16.3–30.9). Patients with acute-on-chronic liver failure showed the highest prevalence of BIs (44.2%; 95% CI: 29.7–59.8). A modest increasing trend in BIs prevalence was observed over time. BIs were associated with an increased risk of mortality in patients with cirrhosis (adjusted hazard ratios 2.22, 95% CI 1.33–3.71).

BIs are prevalent in cirrhosis, especially in acute-on-chronic liver failure, with a modest upward trend and increased mortality risk.

Chimeric antigen receptor (CAR)-T cell therapy faces significant challenges in treating solid tumors, including immune evasion, suppressive tumor microenvironments, and on-target/off-tumor toxicity, which limit its clinical efficacy. Although it has revolutionized treatment for hematological malignancies, these obstacles hinder its broader application in solid tumors. Nanotechnology offers innovative strategies to address these limitations through enhanced delivery, localization, and control. This review summarizes recent advances in nanotechnology-assisted CAR-T cell therapies for gynecologic cancers, with a particular focus on messenger RNA (mRNA)-based delivery systems, lipid nanoparticles, hydrogels, and external activation techniques such as photothermal and acoustogenetic modulation. The integration of nanotechnology, especially mRNA-based delivery systems, holds transformative potential for overcoming these barriers. mRNA enables transient, non-integrating expression of CARs, meaning the genetic modifications are temporary. This improves safety and allows flexible control over treatment intensity, while rational sequence optimization (e.g., codon usage, guanine-cytosine content, secondary structure) enhances mRNA stability and protein translation efficiency. Lipid nanoparticles, the leading delivery platform, can be engineered for cell-type specificity and tissue targeting through modulation of their components and surface functionalization. Recent innovations, including siloxane-modified lipid nanoparticles, injectable hydrogels, and photothermal or acoustogenetic activation strategies, enable precise spatiotemporal control of CAR-T cell function in vivo. In ovarian cancer, preclinical studies targeting nfP2X7 and employing multifunctional nanoparticles have demonstrated synergistic efficacy and tumor-specific delivery. This review highlights how nanotechnology platforms can be integrated with CAR-T cell therapies to enhance safety, precision, and therapeutic outcomes in ovarian cancer.

Familial hypobetalipoproteinemia (FHBL), caused by apolipoprotein B (APOB) variants, disrupts APOB-containing lipoprotein synthesis, leading to reduced serum total cholesterol, low-density lipoprotein cholesterol, and APOB. Heterozygous carriers are often asymptomatic, while homozygotes exhibit severe manifestations like malabsorption, vitamin deficiencies, and hepatic steatosis. In recent years, FHBL has attracted increasing attention due to its association with liver disease and its role as a unique monogenic model of steatotic liver disease independent of cardiometabolic risk factors. Mechanistically, lipid overload, endoplasmic reticulum stress, oxidative damage, and impaired autophagy may drive hepatocellular injury and fibrosis. Challenges include insufficient diagnosis, sparse epidemiological data, and unclear disease progression. Enhanced genetic testing, mechanistic research, and longitudinal studies are critical to improving diagnosis, risk assessment, and therapies for FHBL-associated liver disease.