Chronic heart failure （CHF） refers to a clinical syndrome in which the function or structure of the heart is changed due to damage to the original myocardium， resulting in reduced pumping and/or filling functions of the heart. In recent years， the mechanisms， pathways， and targets of traditional Chinese medicine （TCM） in the treatment of CHF have been continuously confirmed， and the application of TCM theories in guiding the syndrome differentiation and precise treatment of CHF is currently a research hotspot. On the basis of the syndrome differentiation and treatment in TCM， Professor LI Candong innovatively proposed the thinking of five differentiation： Disease differentiation， syndrome differentiation， pathogenesis differentiation， symptom differentiation， and individual differentiation. This article explores the clinical diagnosis and treatment of CHF from this thinking， emphasizing comprehensive syndrome differentiation， objective analysis， dynamic assessment， and individualized treatment. In terms of diagnosis， the first is to identify the disease name， cause， location， severity， and type of CHF， determine the type and its evolution， and clarify the process of transmission and transformation between deficiency and excess. Secondly， it is necessary to distinguish the authenticity， severity， primary and secondary， urgency and complexity of CHF syndromes， providing scientific guidance for syndrome differentiation and treatment. Thirdly， according to the symptoms and the principles of deficiency and excess， the physician should identify the core pathogenesis of CHF from the perspectives of Qi， blood， Yin， Yang， deficiency， stasis， phlegm， water， and toxins. Fourthly， from the macro， meso and micro levels， the physician should carefully distinguish the presence or absence， severity， authenticity， and completeness of the symptoms to guide the diagnosis and treatment process of CHF. Finally， personalized medication for CHF should be promoted based on the patient's gender， age， constitution， and living habits. In terms of treatment， based on the thinking of five differentiation， we propose that the treatment of CHF should integrate the disease and syndrome， clarify the pathogenesis， and apply precise treatment. The treatment should be people-oriented， staged， and typed， and the medication should be adjusted according to symptoms. This diagnostic and therapeutic approach is based on the holistic concept and syndrome differentiation and treatment， and combines the three causes for appropriate treatment， providing new ideas and insights for the diagnosis and treatment of CHF.

OBJECTIVE To analyze the characteristics and influencing factors of disposal behavior of expired medicines among Chinese residents across regional divisions， and to provide references for regional classification management and precise policy implementation regarding expired medicines. METHODS A stratified random sampling method was employed to conduct a questionnaire survey among residents across sample provinces and cities， utilizing a combination of online and offline approaches. Binary Logistic regression analysis was used to systematically explore the regional （eastern， central and western regions） and urban-rural disparities in the recycling of expired medicines among Chinese residents， identify the core driving factors influencing standardized disposal behaviors， and propose corresponding recommendations. RESULTS A total of 2 200 ques tionnaires were collected， with 2 159 deemed valid， yielding an effective response rate of 98.1%. The surveyed residents commonly stored medicines at home （67.7%）， yet the rate of regular medicine clearance was low （only 57.7%）. Nearly half of the residents （49.7%） had expired medicines in their households， with improper disposal of expired medicines remaining the predominant behavior. Insufficient convenience in recycling was identified as the primary reason for improper disposal of expired medicines （50.1%）. Statistically significant differences were observed between residents in the eastern， central and western regions， as well as between urban and rural residents， in terms of household medicine storage rates and the prevalence of expired medicine possession （ P ＜0.05）. However， no statistically significant difference was found in the standardized disposal rates across regional divisions （ P ＞0.05）. Furthermore， the residents demonstrated a higher level of awareness regarding the health hazards of expired medicines compared to their awareness of environmental hazards， with 46.0% and 32.1% indicating they were “relatively familiar” and “very familiar”， respectively. The participation rate in standardized recycling was only 37.6%. Among non-participating residents， the three primary barriers were “recycling points being too far away” （46.6%）， “unawareness of recycling channels” （46.1%） and “lack of incentives” （48.1%）. The surveyed residents showed relatively high trust in pharmaceutical regulatory authorities and on-site recycling personnel， with “high trust” accounting for 31.2% and 34.7%， respectively. Binary Logistic regression analysis results indicated that the awareness of environmental hazards and the accessibility of recycling points were the core driving factors for proper disposal. CONCLUSIONS Significant issues exist in the recycling of expired medicines among Chinese residents， characterized by “improper behavior， cognitive bias， and unbalanced system”. It is recommended to construct a tiered recycling network focusing on “quality improvement in the eastern region， expansion in the central region， and basic coverage in the western region”， implement targeted educational campaigns and differentiated incentive policies. Moreover， the specific needs of groups such as the elderly should be addressed to achieve spatial equalization and service optimization of the recycling system.

The Golgi body, a core organelle in eukaryotic cells, plays a critical role in protein modification, sorting, vesicular transport, and serves as a key site for lipid synthesis and glycosylation. Glucose and lipid metabolism are central processes for cellular energy maintenance and biosynthesis, and are closely linked to Golgi function. Recent studies have revealed the extensive involvement of the Golgi body in regulating glucose and lipid metabolism, where maintaining its structural and functional homeostasis is crucial for normal physiological activity. Under various stress conditions such as acidosis, hypoxia, and nutrient deficiency, the Golgi body undergoes structural and functional disruption, leading to Golgi stress. This in turn activates specific signaling pathways, such as those mediated by the cAMP-responsive element binding protein 3 (CREB3) and proteoglycans, to alleviate Golgi stress and enhance Golgi function. Golgi stress contributes to glucose and lipid metabolic disorders by affecting the activity of insulin receptors, glucose transporters, and lipid metabolism-related enzymes. For example, Golgi stress triggers the cleavage and release of the active fragment of CREB3, which enters the nucleus and upregulates the transcription of ADP-ribosylation factor 4 (ARF4) and key gluconeogenic enzymes, including phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase). ARF4 promotes vesicle retrograde transport between the Golgi and endoplasmic reticulum, maintains secretory capacity, and enhances hepatic glucose output. This pathway is particularly active under high-fat or lipotoxic stress, leading to fasting hyperglycemia. When damaged Golgi components accumulate beyond a tolerable threshold, the cell initiates an autophagic response, selectively encapsulating the damaged Golgi into autophagosomes, which then fuse with lysosomes to form autolysosomes, leading to Golgiphagy. This process results in the degradation and clearance of damaged Golgi, thereby regulating Golgi quantity, quality, and function. Golgiphagy also plays a significant role in regulating glucose and lipid metabolism. For instance, under high-glucose conditions, autophagic flux may be suppressed, impairing the timely clearance and renewal of damaged Golgi, compromising its normal function, and further exacerbating glucose metabolism disorders. Additionally, Golgiphagy may participate in lipid degradation and influence lipid synthesis and transport. Research indicates that Golgi stress and Golgiphagy play important roles in glucose and lipid metabolism-related diseases. For example, the leucine zipper protein (LZIP) under Golgi stress conditions can promote hepatic steatosis. In mouse primary cells and human tissues, LZIP induces the expression of apolipoprotein A-IV (APOA4), which increases peripheral free fatty acid uptake, resulting in lipid accumulation in the liver and contributing to the development of fatty liver disease. This review systematically outlines the structure and function of the Golgi apparatus, the molecular regulatory mechanisms of Golgi stress and Golgiphagy, and their synergistic roles. It further elaborates on how Golgi stress and Golgiphagy participate in the regulation of glucose and lipid metabolism, discusses their clinical significance in related diseases such as diabetes, fatty liver disease, and obesity, and highlights potential novel therapeutic strategies from the perspective of Golgi-targeted medicine. Finally, this article addresses the challenges and future directions in Golgi-targeted interventions, aiming to advance the clinical translation of such strategies and foster breakthroughs in the treatment of glucose and lipid metabolism-related disorders.

The Golgi body, a core organelle in eukaryotic cells, plays a critical role in protein modification, sorting, vesicular transport, and serves as a key site for lipid synthesis and glycosylation. Glucose and lipid metabolism are central processes for cellular energy maintenance and biosynthesis, and are closely linked to Golgi function. Recent studies have revealed the extensive involvement of the Golgi body in regulating glucose and lipid metabolism, where maintaining its structural and functional homeostasis is crucial for normal physiological activity. Under various stress conditions such as acidosis, hypoxia, and nutrient deficiency, the Golgi body undergoes structural and functional disruption, leading to Golgi stress. This in turn activates specific signaling pathways, such as those mediated by the cAMP-responsive element binding protein 3 (CREB3) and proteoglycans, to alleviate Golgi stress and enhance Golgi function. Golgi stress contributes to glucose and lipid metabolic disorders by affecting the activity of insulin receptors, glucose transporters, and lipid metabolism-related enzymes. For example, Golgi stress triggers the cleavage and release of the active fragment of CREB3, which enters the nucleus and upregulates the transcription of ADP-ribosylation factor 4 (ARF4) and key gluconeogenic enzymes, including phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase). ARF4 promotes vesicle retrograde transport between the Golgi and endoplasmic reticulum, maintains secretory capacity, and enhances hepatic glucose output. This pathway is particularly active under high-fat or lipotoxic stress, leading to fasting hyperglycemia. When damaged Golgi components accumulate beyond a tolerable threshold, the cell initiates an autophagic response, selectively encapsulating the damaged Golgi into autophagosomes, which then fuse with lysosomes to form autolysosomes, leading to Golgiphagy. This process results in the degradation and clearance of damaged Golgi, thereby regulating Golgi quantity, quality, and function. Golgiphagy also plays a significant role in regulating glucose and lipid metabolism. For instance, under high-glucose conditions, autophagic flux may be suppressed, impairing the timely clearance and renewal of damaged Golgi, compromising its normal function, and further exacerbating glucose metabolism disorders. Additionally, Golgiphagy may participate in lipid degradation and influence lipid synthesis and transport. Research indicates that Golgi stress and Golgiphagy play important roles in glucose and lipid metabolism-related diseases. For example, the leucine zipper protein (LZIP) under Golgi stress conditions can promote hepatic steatosis. In mouse primary cells and human tissues, LZIP induces the expression of apolipoprotein A-IV (APOA4), which increases peripheral free fatty acid uptake, resulting in lipid accumulation in the liver and contributing to the development of fatty liver disease. This review systematically outlines the structure and function of the Golgi apparatus, the molecular regulatory mechanisms of Golgi stress and Golgiphagy, and their synergistic roles. It further elaborates on how Golgi stress and Golgiphagy participate in the regulation of glucose and lipid metabolism, discusses their clinical significance in related diseases such as diabetes, fatty liver disease, and obesity, and highlights potential novel therapeutic strategies from the perspective of Golgi-targeted medicine. Finally, this article addresses the challenges and future directions in Golgi-targeted interventions, aiming to advance the clinical translation of such strategies and foster breakthroughs in the treatment of glucose and lipid metabolism-related disorders.

Primary cilia—those solitary, microtubule-based projections extending from the surface of most eukaryotic cells—are increasingly recognized not merely as cellular appendages, but as sophisticated signaling hubs. By compartmentalizing specific receptors (e.g., GPCRs) and effectors within a microdomain guarded by the transition zone, these organelles function effectively as high-gain sensors capable of integrating mechanical stimuli with metabolic cues. In this review, we examine the pivotal role of primary cilia across the nervous, bone-vascular, and renal landscapes, arguing for a unified “mechano-metabolic coupling” framework. Here, conserved ciliary modules are not static; rather, they are differentially deployed to uphold systemic homeostasis. Within the central nervous system, we position primary cilia as upstream integrators. We highlight how hypothalamic neuronal cilia concentrate metabolic receptors, such as the melanocortin 4 receptor (MC4R), to interpret energy status. Moreover, the recent identification of serotonergic “axon-cilium synapses” points to a direct mode of neurotransmission, wherein 5-HT6 receptors drive nuclear signaling and chromatin accessibility to rapidly modulate gene expression. Through these mechanisms, central cilia modulate sympathetic tone and neuroendocrine output, effectively establishing the mechanical and metabolic “boundary conditions” under which peripheral organs operate. Dysfunction in these central hubs is linked to obesity and neurodevelopmental disorders, including Bardet-Biedl syndrome. In peripheral tissues, cilia serve as versatile mechanotransducers that convert physical forces into biochemical responses. Regarding the bone-vascular system, we discuss the translation of mechanical loads and fluid shear stress into structural remodeling. In osteoblasts, specifically, ciliary integrity is intrinsically linked to cholesterol and glucose metabolism, fine-tuning the balance between Hedgehog and Wnt/β-catenin signaling to govern osteogenesis and bone repair. A similar dynamic exists in the vasculature, where endothelial cilia sense shear stress to modulate KLF4 expression and endothelial-to-mesenchymal transition—processes critical for valvulogenesis and vascular remodeling. Meanwhile, in the kidney, tubular cilia act as terminal effectors within a “shear-cilia-metabolism” axis. Here, fluid shear stress engages ciliary signaling to trigger AMPK-mediated lipophagy and mitochondrial biogenesis, thereby securing the ATP supply required for solute transport. Notably, dysregulation of this axis leads to metabolic reprogramming and aberrant proliferation, acting as a hallmark driver of cystogenesis in polycystic kidney disease (PKD). Crucially, this review attempts to dissect the often-conflated logic of cross-system integration by distinguishing 3 non-equivalent pathways: direct communication via ciliary extracellular vesicles, though this remains largely hypothetical in long-range signaling; “physiology-mediated cascades”, where ciliary dysfunction in a single organ—such as the kidney—precipitates systemic pathology through hemodynamic and metabolic shifts (e.g., altered blood pressure, fluid volume, or uremic toxins); and “parallel molecular defects”, where shared genetic mutations in ubiquitous components like the IFT machinery cause simultaneous, independent failures across multiple organ systems. Building on these distinctions, we propose a nested-loop model that links central set-points with peripheral feedback via physiological variables. Furthermore, we construct a “causality-to-translation” roadmap that pinpoints structural repair (e.g., targeting IFT assembly) and metabolic rescue (e.g., AMPK activation or autophagy induction) as promising therapeutic avenues. Ultimately, this framework provides a theoretical basis for deciphering the shared pathological mechanisms of multisystem ciliopathies, offering a strategic guide for the development of targeted interventions that go beyond symptomatic treatment.

Dietary interventions such as fasting are gaining increasing attention for their synergistic effects in anti-tumor therapy, yet the precise underlying mechanisms remain incompletely understood. Recent research has unveiled a novel mode of cell death named “mitoxyperilysis”, providing a fresh perspective on the molecular mechanisms by which fasting may interfere with tumor treatment. This form of death is primarily triggered by the synergy between metabolic dysfunction and innate immune activation. Its mechanism involves the mTORC2 signaling pathway mediating prolonged abnormal contact between damaged mitochondria and the plasma membrane. This leads to massive local release of reactive oxygen species (ROS), which further induces lipid peroxidation of the plasma membrane, ultimately resulting in the physical rupture and death of the cell. The most significant distinction between mitoxyperilysis and classical cell death pathways lies in its independence from caspases and GSDMD. This comment aims to systematically elucidate the process, molecular mechanisms, and differences from other classical cell death pathways of mitoxyperilysis, while also exploring its potential for clinical translation in oncological diseases. Targeting induction of mitoxyperilysis may enhance the efficacy of existing anti-tumor drugs and overcome chemotherapy resistance. However, intervention protocols require further optimization to achieve an optimal balance between safety and therapeutic effectiveness in clinical application.

The emergence of immunotherapy has provided new optimism for cancer treatment. Tumor vaccine, a promising immunotherapy strategy, can be categorized into those with identified single or multiple antigens and those with unidentified whole-tumor antigens as their antigenic sources. Currently, mainstream tumor vaccines are still based on identified antigens. However, due to their limitations, tumor vaccines prepared based on whole tumor antigens have unique advantages. However, the low immunogenicity of whole-tumor antigen vaccines affected their clinical efficacy. To improve the immunogenicity, researchers have employed various strategies such as immunogenic death, genetic engineering modifications, cell membrane modifications, and tumor cell lysates, which demonstrated significant clinical potential. The research progress of engineering whole-cell vaccines based on tumor cells in recent years was reviewed in this paper, with a focus on their clinical progress and application prospects.

Objective To investigate occupational exposure levels of lead, arsenic and cadmium in the lead smelting plant of Hunan Shui Kou Shan Nonferrous Metals Group Co. Ltd., analyze their effects on health of employees, and compare the applicability of different occupational health risk assessment methods, and to provide a basis for prevention and control of occupational exposure risks in enterprises. Methods According to systematic sampling method, 380 employees with lead, arsenic and cadmium exposure (exposure group) and 100 non-exposure employees (non-exposure group) were selected from 2022 to 2024 for on-site investigation of occupational health [concentration time-weighted average (C_TWA)] and physical examination. The risk was evaluated by qualitative assessment method, the U.S. Environmental Protection Agency (EPA) inhalation risk assessment method, and the Singapore Ministry of Manpower (MOM) semi-quantitative method. The consistency was analyzed by the Kappa test. Results C_TWA values of lead, arsenic, and cadmium in all positions were lower than the occupational exposure limit (OEL). The levels of blood lead, urine arsenic, and urine cadmium, as well as the prevalence of multiple systems in the exposure group were significantly higher than those in the non-exposure group (P<0.05). The proportions of chronic lead, arsenic, and cadmium poisoning were increasing year by year in the exposure group (P<0.05). The qualitative assessment method mainly indicated low and medium risk, while the EPA and MOM methods mainly indicated medium and high risk, with good agreement between the two methods (Kappa=0.676, P<0.05). Conclusion Although the enterprise meets the C_TWA standards, there are still occupational health risks of lead, arsenic, and cadmium. The EPA inhalation risk assessment method is more applicable.

Antibody-drug conjugates (ADCs) have emerged as a standard treatment modality for previously treated driver gene-positive advanced non-small cell lung cancer (NSCLC). Sacituzumab tirumotecan (sac-TMT), a novel TROP-2-targeting ADC, has been the focus of the phase Ⅲ clinical trial OptiTROP-Lung04. This trial demonstrated, for the first time, that single-agent sac-TMT significantly improves progression-free survival and overall survival compared with conventional platinum-based chemotherapy in patients with epidermal growth factor receptor (EGFR) mutant advanced NSCLC following resistance to EGFR tyrosine kinase inhibitors. This review combines existing consensus from literature with the latest research evidence to systematically analyze OptiTROP-Lung04 from multiple perspectives, including molecular mechanisms, study design, clinical significance, and safety management. Furthermore, it explores future development directions in an effort to provide new insights into precision therapy for advanced NSCLC.

Ferroptosis exhibits a clear “double-edged sword” effect in liver fibrosis， with its impact strictly dependent on the type of target cells. In hepatocytes， ferroptosis induced by specific signaling pathways （such as glutathione peroxidase 4 inhibition） is a key factor for driving hepatic injury and initiating fibrogenesis， and dying hepatocytes activate hepatic stellate cells by releasing damage-associated molecules； on the contrary， in activated hepatic stellate cells， ferroptosis becomes a therapeutic target for promoting liver fibrosis regression， and selective elimination can be achieved by disrupting their distinctive antioxidant defense mechanisms. Moreover， ferroptosis modulates the dynamic balance of the fibrotic liver microenvironment by regulating macrophage polarization and intercellular communication. Based on the above mechanisms， targeting ferroptosis has emerged as a promising strategy for precise treatment. This article summarizes related research advances and discusses the major challenges and future directions for clinical translation.