Numerous liver diseases are characterized by late diagnosis, rapid progression and high incidence, seriously threatening public health. Though widely used, traditional treatments such as drug therapy, resection and transplantation have substantial limitations. Therefore, developing novel preventive strategies and specialized therapies is crucial. As Chinese medicine continues to modernize, increasing evidence suggests that certain Chinese medicine ingredients can protect the liver. Astragaloside IV (AS‑IV) is a natural saponin extracted from the root of the traditional herb Astragalus membranaceous. It exhibits diverse pharmacological activities, including anti‑inflammatory, antioxidant, antiapoptotic and anticancer properties, and is recognized for treating neurological, cardiovascular and metabolic disorders, and cancer. These discoveries indicate its substantial promise for the treatment of liver diseases. Therapeutic trials revealed its hepatoprotective effects for the treatment of various liver diseases, such as non‑alcoholic fatty liver disease, liver fibrosis, hepatocellular carcinoma and liver injury induced by heavy metals, drugs, or alcohol and involve various signaling pathways such as nuclear factor erythroid 2‑related factor 2, toll‑like receptor 4, acetyl‑CoA carboxylase, protein kinase B, nuclear factor κB and adenosine monophosphate‑activated protein kinase. The present study presents a narrative review that comprehensively summarizes existing evidence regarding the therapeutic influence of AS‑IV on diverse liver disorders and deeply analyzes the molecular mechanisms underlying its action in liver disease. The objective is to comprehensively offer insights and references for relevant scientific research and clinical drug development to improve nutritional supplements for liver health.

S100A8/A9 is a key inflammatory protein significantly upregulated during acute myocardial infarction (AMI). Although previous small-scale studies suggest its potential for cardiovascular risk stratification, its long-term prognostic utility-especially compared to established biomarkers like TnI and BNP-lacks validation in large-scale cohorts. To evaluate the long-term prognostic value of admission plasma S100A8/A9 levels in a large cohort of hospitalized AMI patients, specifically assessing its ability to predict major adverse cardiovascular events (MACE) and its incremental predictive value over traditional clinical models.

This prospective study enrolled 1,312 patients hospitalizing with AMI from August 2013 to June 2016. Plasma S100A8/A9 levels were quantified via ELISA at admission. Multivariable Cox regression and restricted cubic splines were utilized to assess the associations of S100A8/A9 levels with MACE and its components including all-cause mortality, hospitalization for heart failure (HF), and recurrent myocardial infarction (MI).

Over a median follow-up period of 2.93 years, 132 deaths occurred, and 392 patients reached the combined endpoint of MACEs. Even after multivariable adjustment for baseline clinical characteristics and established biomarkers, elevated S100A8/A9 levels remained significantly associated with an increased risk of MACE, all-cause mortality, recurrent MI, and hospitalization for HF (all P for trend <0.001). Furthermore, using Cox model-based Harrell's C-index, discrimination for MACE improved from 0.752 in the reference model to 0.822 after addition of log-transformed S100A8/A9, but not for all-cause mortality, as reflected in C-index (0.718 to 0.720), with bootstrap ΔC-index 0.002 (95% CI: -0.005, 0.013; P=0.58).

Plasma S100A8/A9 concentrations demonstrate a strong correlation with heightened risk of MACE in AMI patients. Notably, the prognostic value of S100A8/A9 is significantly more pronounced for composite cardiovascular outcomes (MACE) compared to all-cause mortality. These findings indicate that S100A8/A9 serves as a valuable novel biomarker to guide targeted risk stratification of post-AMI patients.

Atrial fibrillation (AF) is a major cause of cardioembolic stroke and often remains undiagnosed because of its asymptomatic or paroxysmal nature. Although opportunistic AF screening has been advocated, sustainable community-based screening models that link the results to medical evaluations are limited. We implemented a pharmacy-based AF screening initiative (Catch AF project) led by a regional Stroke and Cardiovascular Disease Support Center with community pharmacists and physicians to assess its feasibility and follow-up outcomes.

The Catch AF project was conducted at 34 community pharmacies in Nagasaki, Japan. A single-lead electrocardiogram (ECG) device with automated analysis was installed to offer opportunistic screening for pharmacy visitors. Of the 5,371 ECG recordings, 123 (2.29%) indicated possible AF. Pharmacists recommended medical consultation for 60 individuals (49% of the detected cases). Questionnaire surveys demonstrated that stakeholders generally perceived the initiative as acceptable and feasible. In contrast, only a small number of physicians reported encounters with referred patients, indicating a marked gap between AF detection through pharmacy-based screening and subsequent medical evaluation.

A center-led pharmacy-based AF screening initiative is feasible and well accepted in a real-world setting. However, a substantial gap between screening detection and clinical follow up highlights the need for improved referral pathways and coordination between pharmacies and medical institutions to enhance the effectiveness of community-based screening programs.

We aimed to elucidate the characteristics and prognosis of patients admitted to a medical intensive care unit (ICU) by helicopter emergency medical service (HEMS).

Among 11,140 patients transported via the institute's HEMS from January 2012 to December 2021, 459 were admitted to the medical ICU and included as the HEMS group. The 3,810 patients who were transported by other means to the medical ICU comprised the non-HEMS group. Multivariable logistic regression analysis revealed that cardiovascular etiologies other than acute heart failure (AHF), as well as younger age and the requirement of mechanical support (endotracheal intubation and intra-aortic balloon pumping), were associated with HEMS transport. Kaplan-Meier curve analysis revealed that 365-day survival was significantly better in the HEMS group than in the non-HEMS group. A multivariable Cox regression model identified HEMS transport as an independent predictor of a favorable 365-day all-cause survival (hazard ratio: 1.326, 95% confidence interval: 1.024-1.718, P=0.033) relative to other means of transport.

Cardiovascular diseases other than AHF were the main reasons for helicopter transportation to the medical ICU. The HEMS group were younger and more likely to require circulatory/respiratory assist devices than the non-HEMS group. The HEMS was significantly associated with better 365-day survival; therefore, appropriate transportation means need to be selected to improve the prognosis of non-surgical patients.

Low-density lipoprotein cholesterol (LDL-C) is an established therapeutic target for atherosclerotic cardiovascular diseases (ASCVD), particularly in high-risk individuals. In 2022, the Japan Atherosclerosis Society Guidelines (JAS-GL) for Prevention of Atherosclerotic Cardiovascular Diseases introduced more stringent LDL-C targets to reduce ASCVD. We evaluated the non-achievement rates of the LDL-C goals across risk groups using a nationwide real-world dataset, which included a broad range of ASCVD patients.

This retrospective, cross-sectional study included 200,607 adults (aged ≥18 years) with dyslipidemia. Patients were stratified according to the JAS-GL 2022 into a high-risk primary prevention population (Groups I, II, and familial hypercholesterolemia [FH]: no history of coronary artery disease [CAD] or stroke, classified by comorbidities such as diabetes), and a secondary prevention population (Groups III and IV: history of CAD or stroke, with Group IV having additional conditions such as diabetes). The primary endpoint was the proportion of patients who did not achieve their target LDL-C goals. Non-achievement rates were 28.2% (Group I), 46.7% (Group II), 64.3% (Group FH), 30.0% (Group III), and 65.6% (Group IV). Importantly, these rates remained high and showed little change before and after the revision of the guidelines across all studied risk groups.

Non-achievement of LDL-C targets remained high despite updated recommendations. These findings highlight a need for more effective implementation strategies and sustained efforts to improve lipid management.

Cardiovascular disease (CVD) is the leading global cause of death. "Medicine-food homology" (MFH), a fundamental principle of traditional Chinese medicine (TCM), emphasizes dual nutritional and therapeutic roles of natural substances, thereby attracting increasing attention in disease management. These substances exhibit synergistic effects through multiple targets and signaling pathways, demonstrating significant potential in the prevention, adjuvant therapy, and rehabilitation of CVD. This review presents the mechanisms underlying MFH substances (such as astragalus, codonopsis, and hawthorn) in targeting key pathways related to CVD, and summarizes findings from clinical randomized controlled trials (RCT). This review summarizes MFH substances' role in CVD management, focusing on four core mechanisms (vascular defense, myocardial protection, gut-heart axis regulation, risk factor control) that mediate their multi-targeted, multi-pathway effects (e.g., anti-inflammation via Astragalus, myocardial repair via Ginseng). Clinical evidence confirms MFH substances enhance CVD therapeutic efficacy as adjuvant therapies, with mild adverse reactions, while highlighting the need for further research to advance translational application. Future research should prioritize large-scale multi-center trials, multi-omics integration, and standardized quality control to advance MFH from empirical use to precision medicine, providing new natural product-based strategies for comprehensive CVD prevention and treatment.

Salvia miltiorrhiza-Dalbergia odorifera (SM-DO) is a commonly used herb pair for treating cardiovascular diseases. It can treat myocardial infarction (MI) by regulating glycolysis and angiogenesis, but the optimal proportion of its active components remains unclear.

Based on the enhanced simplex-centroid mixture design using Minitab 19 software, 19 proportions of salvianolic acid B (Sal-B), butein (But), tanshinone IIA (Tan IIA), and formononetin (For) were applied to an oxygen-glucose deprivation (OGD)-treated human cardiac microvascular endothelial cells (HCMVECs)-AC16 cells co-culture system. The proportions were independent variables, and viability, lactic acid, vascular endothelial growth factor (VEGF) of HCMVECs, and cardiac troponin I (cTnI) of AC16 cells were dependent variables. Regression equations were fitted and multi-objective optimization was performed to determine the OP, and experimental verification was conducted.

Stepwise regression analysis yielded regression equations for the four response indicators. The R ² and adjusted R ² of each model were at reasonable levels, and the predicted R ² showed no significant decay. Multi-objective simultaneous optimization revealed OP of 60% Sal-B, 5% But, 5% Tan IIA, and 30% For. Experimental validation results showed that OP could promote lactic acid and VEGF production in OGD HCMVECs, enhance HCMVEC viability, and inhibit cTnI release in OGD AC16 cells. In vivo, OP increased levels of lactic acid, total protein lactylation (Pan-Kla), and VEGF in the myocardium of MI mice, and decreased levels of cTnI, creatine kinase-myocardial band (CK-MB), and myoglobin (Myo) in serum, alleviated pathological injury and fibrosis in myocardial tissues, and enhanced cardiac function in mice.

This study preliminarily clarifies the OP composed of Sal-B, But, Tan IIA, and For that improves glycolysis and angiogenesis-related indicators and exerts cardioprotective effects, providing a new strategy for studies on active component formulations of traditional Chinese medicines. It is expected to lay a methodological foundation for the clinical application of SM-DO and the development of new drugs.

Matrine is the main active metabolite of Sophora flavescens Ait. Matrine is a traditional medicine with a long history of medicinal use. Modern pharmacological research confirms that matrine possesses a variety of pharmacological effects, including anti-inflammatory, immunomodulatory, and anti-parasitic activities. Ferroptosis is a form of programmed cell death characterized by iron accumulation and lipid peroxidation. Recent studies show that matrine achieves organ protection or therapeutic effects in various diseases by regulating the shared pathway of ferroptosis. This review explores the multi-target intervention role of matrine in cardiovascular diseases, central nervous system diseases, acute lung injury induced by severe acute pancreatitis, and cervical cancer through the mechanism of ferroptosis. By comparing and deeply analyzing different research findings, the review provides a theoretical basis for future research and potential drug development. It also integrates existing preclinical evidence and emphasizes the need for rigorous, multi-center, and large-scale clinical studies to accelerate the translation of matrine from the laboratory to clinical practice. The cross-disease therapeutic potential of matrine via ferroptosis regulation positions it as a candidate molecule linking the multi-target advantages of natural metabolites with modern precision medicine. However, its dose-dependent tissue toxicity necessitates that future research integrate derivative optimization, targeted delivery systems, and biomarker-based individualized dosing strategies to achieve a safe transition from laboratory to clinical practice.

Age-associated B cells (ABCs) are a B-cell subset with distinct transcription and functional properties. Their functions include antibodies secretion, cytokine production, antigen presentation and T-cell stimulation. ABCs have been found expanded in aging, infections and autoimmune diseases such as systemic lupus erythematous, multiple sclerosis and rheumatoid arthritis (RA). ABCs have emerged as plausible mediators of autoimmunity by virtue of their ability to produce autoantibodies and proinflammatory cytokines, as well as trigger T-cell activation, although mechanisms may differ across diseases. Moreover, ABCs may represent a mechanistic link between immunosenescence, premature aging and disease outcomes. Herein, we describe the current knowledge of ABCs in RA with a special focus in the early stages and comorbidity development. Accumulating evidence from preclinical and clinical studies with RA patients have demonstrated disturbances within the ABCs pool. Animal models suggest that ABCs play an important role already in the early phases of the disease and data from RA patients seem to support this hypothesis. Besides, RA risk factors and disease activity may be linked to ABCs expansion, which is associated with high levels of proinflammatory cytokines and correlated with skewed helper T-cell profiles, potentially contributing to inflammaging. Moreover, ABCs may not only be involved in the RA immunopathology, but also in the clinical expression of this disease at synovial and systemic levels. Potential roles of ABCs in cardiovascular, lung, neurological, kidney and metabolic comorbidities are identified, although level of evidence is heterogeneous and limited in some cases. Future perspectives for research, clinical translation and therapeutic implications are discussed.

Endothelial cells (ECs) sense hemodynamic forces and critically influence aortic aneurysm and dissection (AAD) development. However, the possible contribution of the mechanical sensor Piezo1 to AAD remains elusive. Single-cell mRNA sequencing identified Piezo1 as the most up-regulated mechanical sensor in ECs from AAD model mice. Immunofluorescence and immunoblotting confirmed markedly increased Piezo1 protein in human and mouse AAD samples. Disturbed flow induced by abdominal aortic constriction plus Angiotensin II up-regulated Piezo1 expression and AAD incidence, whereas Piezo1 inhibition attenuated both. Moreover, EC-specific Piezo1 deficiency was sufficient to suppress β-aminopropionitrile- and Ang II-induced AAD formation in mice. Mechanistically, we discovered the disturbed shear stress-induced opening of the endothelial barrier via Piezo1 and subsequent Ca²⁺/MLC/PYK2/SRC-mediated activation of downstream signaling. In addition, in an Ang II-induced endothelial barrier dysfunction model, Piezo1 deficiency in ECs ameliorated Ang II-induced barrier dysfunction. Further study revealed that Piezo1 activation in ECs promoted the up-regulation of CCL2 in a STAT3-dependent manner and strongly promoted the chemotactic recruitment of monocytes/macrophages to the aorta. Importantly, blocking CCR2 reduced monocyte/macrophage recruitment and subsequently attenuated Piezo1 up-regulation-aggravated AAD formation. Transcriptome analysis of human AAD samples revealed a positive correlation between Piezo1 and inflammation of the aorta. We demonstrate that Piezo1 directly links mechanical sensing under disturbed flow to a pathogenic cascade of endothelial barrier dysfunction and inflammatory cell recruitment. Consequently, interventions targeting Piezo1 or the downstream STAT3-CCL2/CCR2 signaling hold therapeutic promise for AAD.