Cardiovascular diseases， a group of major non-infectious diseases， are characterized by high morbidity and mortality， significantly influencing patients' quality of life. Hence， it is imperative to discover a secure and efficacious treatment approach. As a form of programmed cell death， autophagy has been demonstrated to be associated with the pathogeneses of hypertension， diabetic cardiomyopathy， myocardial ischemia-reperfusion injury， heart failure， atherosclerosis， and other cardiovascular disorders. It serves as one of the potential targets for the clinical intervention in cardiovascular diseases by traditional Chinese medicine （TCM）. Autophagy exerts dual regulatory effects on the occurrence and development of cardiovascular diseases， and its specific effect predominantly depends on the extent of autophagy and the pathological stage of diseases. Recent studies have confirmed that TCM can prevent and treat cardiovascular diseases by directly regulating autophagy or interacting with oxidative stress， inflammation， and apoptosis under the regulation of autophagy， exhibiting the unique advantages of multiple targets， multiple components， and mild adverse reactions. This article reviews the experimental research progress in the role of autophagy and the intervention by active components and compound prescriptions of TCM and Chinese patent medicines in common cardiovascular diseases （such as diabetic cardiomyopathy， myocardial ischemia-reperfusion injury， heart failure， and atherosclerosis） in recent years and summarizes the research shortcomings， providing a theoretical basis and strategies for the clinical treatment of cardiovascular diseases.

Cardiovascular diseases， a group of major non-infectious diseases， are characterized by high morbidity and mortality， significantly influencing patients' quality of life. Hence， it is imperative to discover a secure and efficacious treatment approach. As a form of programmed cell death， autophagy has been demonstrated to be associated with the pathogeneses of hypertension， diabetic cardiomyopathy， myocardial ischemia-reperfusion injury， heart failure， atherosclerosis， and other cardiovascular disorders. It serves as one of the potential targets for the clinical intervention in cardiovascular diseases by traditional Chinese medicine （TCM）. Autophagy exerts dual regulatory effects on the occurrence and development of cardiovascular diseases， and its specific effect predominantly depends on the extent of autophagy and the pathological stage of diseases. Recent studies have confirmed that TCM can prevent and treat cardiovascular diseases by directly regulating autophagy or interacting with oxidative stress， inflammation， and apoptosis under the regulation of autophagy， exhibiting the unique advantages of multiple targets， multiple components， and mild adverse reactions. This article reviews the experimental research progress in the role of autophagy and the intervention by active components and compound prescriptions of TCM and Chinese patent medicines in common cardiovascular diseases （such as diabetic cardiomyopathy， myocardial ischemia-reperfusion injury， heart failure， and atherosclerosis） in recent years and summarizes the research shortcomings， providing a theoretical basis and strategies for the clinical treatment of cardiovascular diseases.

Sarcopenia is a systemic disease characterized by accelerated loss of skeletal muscle mass and function,leading to an increased incidence of adverse outcomes such as falls and fractures.Sarcopenia is classified into primary and secondary types,with primary sarcopenia being closely related to aging and posing a serious threat to a healthy life among the elderly.Sarcopenia has an insidious onset and is often overlooked in terms of its clinical treatment.Its pathogenesis is complex,involving functional changes and pathological alterations in multiple systems,and presenting major research challenges.Cell models can effectively be used to simulate the pathological changes of diseases under controllable conditions,thus facilitating the investigation of the etiology and factors influencing sarcopenia,and providing an important approach for in-depth studies of its mechanism;however,there is currently no standardized cell model in the field of sarcopenia research.Commonly used cell models currently include models involving protein metabolism interventions,oxidative stress,and inflammatory response interventions.This review considers the commonly used skeletal muscle cell types and modeling method of sarcopenia,to provide a solid foundation and important method ological reference for further simulation of the pathological process of sarcopenia in subsequent experimental studies.

Vascular cognitive impairment(VCI)is a syndrome of cognitive decline attributed to vascular risk factors and cerebrovascular diseases.A range of pathophysiological processes induced by vascular injury,including inflammation,oxidative stress,cell death,disruption of the blood-brain barrier,and synaptic damage are intricately linked to the development of VCI.Nuclear factor E2-related factor 2(Nrf2),encoded by the NFE2L2 gene,is a potent transcription factor that plays a critical role in antioxidant defense.Extensive research has demonstrated that Nrf2 mitigates oxidative stress and inflammation by upregulating the expression of antioxidant response elements,thereby reducing the production of reactive oxygen species.Nrf2 also modulates programmed cell death,enhances blood-brain barrier integrity,and promotes synaptic plasticity,ultimately delaying the progression of VCI.This review examines the role of Nrf2 in VCI and highlights recent research on traditional Chinese medicines targeting Nrf2 for the prevention and treatment of VCI,thus providing novel insights and approaches for managing this condition.

ObjectiveTo evaluate the clinical efficacy and safety of Baoshen prescription in the treatment of stage Ⅳ diabetic nephropathy （DN） in the patients with syndromes of Qi-Yin deficiency and kidney collateral stasis and obstruction， and to explore the mechanism of this prescription delaying the disease progression. MethodsA randomized， controlled， double-blind， multicenter clinical trial was conducted， in which 94 stage Ⅳ DN patients with syndromes of Qi-Yin deficiency and kidney collateral stasis and obstruction were randomly assigned into Baoshen prescription and control groups （47 cases）. The treatment lasted for 12 weeks. The primary efficacy indicators were mainly renal function indexes， including urine albumin-to-creatinine ratio （UACR）， 24-hour urine total protein （24 h-UTP）， serum creatinine （SCr）， and estimated glomerular filtration rate （eGFR）. The secondary efficacy indicators were metabolic memory of hyperglycemia， podocyte epithelial-to-mesenchymal transdifferentiation-related indexes， and TCM syndrome score. ResultsAfter 12 weeks of treatment， the Baoshen prescription group showed lowered levels of advanced glycation end products （lgAGEs）， connective tissue growth factor （CTGF）， type Ⅳ collagen （Col-Ⅳ）， receptor of AGEs （RAGE）， urinary fibroblast-specific protein-1 （FSP-1）， UACR， 24 h-UTP， and glycated hemoglobin （HbAlc） （P<0.05）， and an upward trend of miR-21 mRNA. The control group showed elevated levels of SCr and UREA and lowered levels of urinary FSP-1， eGFR， and HbAlc （P<0.05）. After treatment， the Baoshen prescription group had lower levels of lgAGEs， CTGF， urinary FSP-1， SCr， UACR， and 24 h-UTP and higher levels of Col-Ⅳ and eGFR than the control group （P<0.05）. In addition， the Baoshen prescription group showed statistically significant differences in SCr， eGFR， UACR， and 24 h-UTP before and after treatment （P<0.05）. ConclusionBaoshen prescription can effectively improve the renal function， reduce the urinary protein level， and alleviate clinical symptoms in stage Ⅳ DN patients with syndromes of Qi-Yin deficiency and kidney collateral stasis and obstruction. The mechanism may be related to the metabolic memory of hyperglycemia and epithelial-to-mesenchymal transdifferentiation of podocytes.

Since the introduction of monoamine oxidase and monoamine neurotransmitter reuptake inhibitors for the treatment of major depression in the 1950s, their strengths and limitations have been fully and accurately determined. Therefore, the development of novel drugs for the treatment of depression has become a priority for researchers who aim to address treatment resistance and improve patient outcomes. Panax ginseng C. A. Mey (P. ginseng, Ren Shen) is a Chinese medicine used to treat neurological and psychiatric disorders. Numerous studies have shown that ginsenosides, the primary active constituents of P. ginseng, exert a wide range of effects on the central nervous system. Recent studies have demonstrated that ginsenosides possess significant antidepressant properties in animal models. Ginsenosides, such as Rb1 and Rg1, are steroidal molecules, and steroid derivatives have been successfully used in anesthesia, epilepsy, and more recently, postpartum depression treatment. Based on these findings, ginsenosides are promising candidates for the treatment of depression. This raises the following question: What are the prospects of using ginsenosides to treat depression? To gain a clearer understanding, this review provides a comprehensive analysis of recent research on the antidepressant potential of ginsenosides, along with insights and suggestions for future development in this field.

Objective To elucidate the molecular mechanism of shugan formula in regulating intestinal flora in liver cancer using network pharmacology.Methods The active components and targets of shugan formula were screened using the TCMSP and BATMAN-TCM databases.Targets associated with liver cancer and intestinal flora were extracted from the GeneCards and OMIM databases.The in-tersection targets between the drug and disease were identified using a Venn diagram.Kyoto Encyclopedia of Genes and Genomes(KEGG)and Gene Ontology(GO)enrichment analysis were performed on the intersection targets.Molecular docking technology was em-ployed to validate the binding activities of key components,such as quercetin,kaempferol,with core targets,including TP53 and STAT3.The correlation between targets and the prognosis of liver cancer was assessed through survival analysis.Results KEGG enrichment anal-ysis indicated that shugan formula was primarily enriched in pathways such as cancer pathways.GO enrichment analysis suggested its in-volvement in regulating processes like apoptosis.Molecular docking demonstrated stable binding between key components and core targets.Survival analysis revealed that high expression of tumor protein p53gene(TP53)shortened the overall survival of liver cancer patients,whereas high expression of signal transducer and activator of transcription 3(STAT3)prolonged survival.Conclusion Shugan formula may upregulate STAT3 expression,inhibit TP53 expression,modulate relevant signaling pathways,improve the structure of intestinal flora in liver cancer,and thereby inhibit the proliferation and metastasis of liver cancer cells.

Atherosclerosis(AS)is a chronic inflammatory disease involving various immune cells and is char-acterized by lipid deposition and inflammatory response.In recent years,the field of exosome research has been rapidly developed,thereby enhancing our comprehension of their role in AS.Immune cell-derived exosomes are extracellular vesi-cles secreted by immune cells that possess specificity,stability,and biocompatibility.These exosomes have the capacity to induce diverse responses including modulating gene transcription and regulating cytokine production,thereby influenc-ing the body's inflammatory and immune response.During AS progression,these exosomes primarily participate in patho-logical processes including endothelial dysfunction,lipid deposition,vascular calcification,and plaque rupture,all of which significantly influence the development of AS.This review is focused on exploring the role of exosomes derived from monocytes,macrophages,neutrophils,lymphocytes,as well as other immune cells(neutrophils,eosinophils,mast cells,and myeloid-derived suppressor cells)in AS,aiming to offer insights for diagnosis and clinical treatment.

Sarcopenia is a systemic disease characterized by accelerated loss of skeletal muscle mass and function,leading to an increased incidence of adverse outcomes such as falls and fractures.Sarcopenia is classified into primary and secondary types,with primary sarcopenia being closely related to aging and posing a serious threat to a healthy life among the elderly.Sarcopenia has an insidious onset and is often overlooked in terms of its clinical treatment.Its pathogenesis is complex,involving functional changes and pathological alterations in multiple systems,and presenting major research challenges.Cell models can effectively be used to simulate the pathological changes of diseases under controllable conditions,thus facilitating the investigation of the etiology and factors influencing sarcopenia,and providing an important approach for in-depth studies of its mechanism;however,there is currently no standardized cell model in the field of sarcopenia research.Commonly used cell models currently include models involving protein metabolism interventions,oxidative stress,and inflammatory response interventions.This review considers the commonly used skeletal muscle cell types and modeling method of sarcopenia,to provide a solid foundation and important method ological reference for further simulation of the pathological process of sarcopenia in subsequent experimental studies.

Vascular cognitive impairment(VCI)is a syndrome of cognitive decline attributed to vascular risk factors and cerebrovascular diseases.A range of pathophysiological processes induced by vascular injury,including inflammation,oxidative stress,cell death,disruption of the blood-brain barrier,and synaptic damage are intricately linked to the development of VCI.Nuclear factor E2-related factor 2(Nrf2),encoded by the NFE2L2 gene,is a potent transcription factor that plays a critical role in antioxidant defense.Extensive research has demonstrated that Nrf2 mitigates oxidative stress and inflammation by upregulating the expression of antioxidant response elements,thereby reducing the production of reactive oxygen species.Nrf2 also modulates programmed cell death,enhances blood-brain barrier integrity,and promotes synaptic plasticity,ultimately delaying the progression of VCI.This review examines the role of Nrf2 in VCI and highlights recent research on traditional Chinese medicines targeting Nrf2 for the prevention and treatment of VCI,thus providing novel insights and approaches for managing this condition.