Renal fibrosis （RF） is the primary pathological feature of chronic kidney disease （CKD） progression to end-stage renal disease （ESRD）， with glomerulosclerosis and tubulointerstitial fibrosis as core pathological manifestations. It involves abnormal accumulation of extracellular matrix （ECM） components such as collagen and fibronectin， ultimately leading to structural destruction and functional losses of the kidneys. Sirtuins （SIRTs）， a class of nicotinamide adenine dinucleotide （NAD+）-dependent deacetylases， play crucial roles in cellular metabolism， oxidative stress responses， inflammation regulation， and cell survival. In mammals， there are seven distinct SIRT members （SIRT1 to SIRT7）， which collectively ameliorate RF progression through multiple pathways. These include regulating the transforming growth factor （TGF）-β/Smad signaling pathway， suppressing inflammatory responses， reducing oxidative stress， modulating mitochondrial and autophagy functions， and promoting fatty acid oxidation. In recent years， traditional Chinese medicine （TCM） and its active components have demonstrated significant potential in activating or modulating the SIRT protease family and its regulatory networks to ameliorate RF in a multi-target and holistic manner. However， systematic reviews in this area remain lacking. This article elucidates the mechanisms by which the SIRT protease family regulates RF and reviews the latest research advances in TCM modulation of SIRTs for the prevention and treatment of RF， aiming to provide new insights and approaches for the TCM treatment of RF.

Diabetic kidney disease （DKD） is one of the more common chronic kidney diseases，and its causes are complex. DKD is very easy to progress to end-stage renal disease，and the current therapeutic effect still needs to be improved. As an important excretive organ of the human body， the kidney has physiological functions such as discharging metabolic waste， regulating fluid balance， and maintaining the stability of the body's internal environment. These highly complex biochemical processes all depend on the energy support provided by mitochondria. Mitochondrial dysfunction is a key factor causing kidney injury， and the imbalance of mitochondrial homeostasis is an important link leading to mitochondrial dysfunction. The occurrence and development of DKD are often accompanied by the imbalance of mitochondrial homeostasis in renal cells. Mitochondrial autophagy， as a means of regulating mitochondrial homeostasis， is very important for the prevention and treatment of DKD. The PTEN-induced putative kinase 1 （PINK1）/Parkin pathway is one of the most classical pathways to regulate mitochondrial autophagy. Recent studies have found that some drugs can regulate the PINK1/Parkin signaling pathway to target mitochondrial homeostasis and exert renoprotective effects. In particular， traditional Chinese medicine has a significant effect on early and middle stage DKD by regulating PINK1/Parkin pathway-mediated mitochondrial autophagy. This article discussed the mechanism of PINK1/Parkin pathway in mitochondrial autophagy and DKD and reviewed the effect of PINK1/Parkin pathway-mediated mitochondrial autophagy on DKD. At the same time， it explored the therapeutic effect of traditional Chinese and western medicine on DKD mediated by PINK1/Parkin-mediated mitochondrial autophagy， aiming to broaden the ideas of traditional Chinese and western medicine for the prevention and treatment of DKD from the perspective of PINK1/Parkin regulating mitochondrial autophagy.

Diabetic kidney disease （DKD） is one of the more common chronic kidney diseases，and its causes are complex. DKD is very easy to progress to end-stage renal disease，and the current therapeutic effect still needs to be improved. As an important excretive organ of the human body， the kidney has physiological functions such as discharging metabolic waste， regulating fluid balance， and maintaining the stability of the body's internal environment. These highly complex biochemical processes all depend on the energy support provided by mitochondria. Mitochondrial dysfunction is a key factor causing kidney injury， and the imbalance of mitochondrial homeostasis is an important link leading to mitochondrial dysfunction. The occurrence and development of DKD are often accompanied by the imbalance of mitochondrial homeostasis in renal cells. Mitochondrial autophagy， as a means of regulating mitochondrial homeostasis， is very important for the prevention and treatment of DKD. The PTEN-induced putative kinase 1 （PINK1）/Parkin pathway is one of the most classical pathways to regulate mitochondrial autophagy. Recent studies have found that some drugs can regulate the PINK1/Parkin signaling pathway to target mitochondrial homeostasis and exert renoprotective effects. In particular， traditional Chinese medicine has a significant effect on early and middle stage DKD by regulating PINK1/Parkin pathway-mediated mitochondrial autophagy. This article discussed the mechanism of PINK1/Parkin pathway in mitochondrial autophagy and DKD and reviewed the effect of PINK1/Parkin pathway-mediated mitochondrial autophagy on DKD. At the same time， it explored the therapeutic effect of traditional Chinese and western medicine on DKD mediated by PINK1/Parkin-mediated mitochondrial autophagy， aiming to broaden the ideas of traditional Chinese and western medicine for the prevention and treatment of DKD from the perspective of PINK1/Parkin regulating mitochondrial autophagy.

Breast cancer is the leading cause of cancer-related mortality among women worldwide and has drawn extensive research attention.Owing to its molecular heterogeneity,drug resistance,and low therapeutic response,single-modality treatments often fail to achieve satisfactory efficacy or broad applicability.Combination therapy,designed based on the pathophysiological characteristics,related signaling pathways,and biomarkers of breast cancer,has emerged as a promising approach for improving therapeutic outcomes.With the advancement of research on combination strategies,the understanding of their molecular mechanisms—particularly key signaling pathways and biomarkers—has become increasingly important.However,comprehensive reviews addressing these molecular mechanisms and synergistic strategies remain scarce.This article summarizes recent advances in combination therapy for breast cancer,providing a comprehensive review of recent combination therapies for breast cancer and their underlying molecular mechanisms,and focusing on key signaling pathways involved in combination therapy and synergistic strategies,thereby providing theoretical insights and reference for researchers,graduate students,and clinicians engaged in the development of novel combination therapeutic strategies for breast cancer and related malignancies.

Breast cancer is the leading cause of cancer-related mortality among women worldwide and has drawn extensive research attention.Owing to its molecular heterogeneity,drug resistance,and low therapeutic response,single-modality treatments often fail to achieve satisfactory efficacy or broad applicability.Combination therapy,designed based on the pathophysiological characteristics,related signaling pathways,and biomarkers of breast cancer,has emerged as a promising approach for improving therapeutic outcomes.With the advancement of research on combination strategies,the understanding of their molecular mechanisms—particularly key signaling pathways and biomarkers—has become increasingly important.However,comprehensive reviews addressing these molecular mechanisms and synergistic strategies remain scarce.This article summarizes recent advances in combination therapy for breast cancer,providing a comprehensive review of recent combination therapies for breast cancer and their underlying molecular mechanisms,and focusing on key signaling pathways involved in combination therapy and synergistic strategies,thereby providing theoretical insights and reference for researchers,graduate students,and clinicians engaged in the development of novel combination therapeutic strategies for breast cancer and related malignancies.

BACKGROUND:Combined radiation and wound injury appeared mainly in patients with tumor radiotherapy and nuclear radiation accidents.The radiation destroys the repair mechanism,resulting in delayed or prolonged wound healing.It still lacks an effective therapeutic strategy currently. OBJECTIVE:To prepare multifunctional wound dressings based on the multiple clinical symptoms of combined radiation and wound injury,which are designed to be antibacteria,promoted healing and analgesics. METHODS:Using levofloxacin,fibroin and lidocaine hydrochloride as raw materials,3D bioprinting technology was applied to prepare the multifunctional wound dressing.(1)The multifunctional dressing was placed on a fixed culture plate coated with Staphylococcus aureus,Escherichia coli and Pseudomonas aeruginosa,and incubated at 37 ℃ overnight to detect the diameter of the antibacterial zone.(2)40 Kunming mice were randomly divided into trauma group,radiation and trauma model group,treatment group and positive drug group,with 10 mice in each group.Mice in the radiation and trauma model group,treatment group and positive drug group were irradiated by 60Co gamma rays.After 1 hour of radiation,a full-layer skin defect wound with a diameter of 1 cm was made on the back of each mouse in the four groups.Normal saline was applied to the wounds of the trauma group and the radiation and trauma model group.Trethanolamine cream was applied to the wounds of the positive drug group.Multifunctional dressing was applied to the wounds of the treatment group.The dressing was changed every 2 days,and the treatment was continued for 14 days.Wound healing rate and serum interleukin-6 level were measured at 3,7 and 14 days after wound modeling.14 days after the wound modeling,the skin tissue of the wound was obtained and received hematoxylin-eosin staining,Masson staining and cytokeratin-14 immunohistochemical staining. RESULTS AND CONCLUSION:(1)3D-printed multifunctional wound dressing had good antibacterial activity.The antibacterial zone diameters against Staphylococcus aureus,Escherichia coli and Pseudomonas aeruginosa were(4.15±0.09),(4.18±0.23)and(4.35±0.13)cm,respectively.(2)With the extension of modeling time,the wound healed gradually.The wound healing rate of the treatment group and the positive drug group was higher than that of the radiation and trauma model group at 3,7 and 14 days after modeling(P<0.01,P<0.001).The wound healing rate of the treatment group was higher than that of the positive drug group.With the extension of modeling time,the serum interleukin level of mice increased first and then decreased.The serum interleukin level in the treatment group at 3,7 and 14 days after modeling was lower than that in the radiation and trauma model group.Hematoxylin-eosin staining and Masson staining exhibited that inflammatory cells infiltrated the granuloma tissue in the trauma group,and the dermal collagen fibers were densely arranged.The normal structure of epidermis and dermis was destroyed and inflammatory cells were infiltrated in the radiation and trauma model group.In the treatment group,normal skin mucosal tissue was observed,the epidermis was arranged closely,and the sweat glands,hair follicles and dermal collagen fibers were arranged regularly.In the positive drug group,the arrangement of epidermal layer was tight,and the arrangement of sweat glands,hair follicles and dermal collagen fibers was regular.Cytokeratin-14 immunohistochemical staining displayed that the epidermal tissue thickness in the treatment group was lower than that in the other three groups(P<0.01,P<0.001).(3)The results confirm that the 3D-printed multifunctional dressing has multiple functions of local anesthesia,anti-infection and promoting healing.

The heavily harsh plateau environment including low pressure, hypoxia, cold, dryness and strong ultraviolet radiation, seriously threatens the physical and mental health of those who quickly enter the plateau area. Lungs are the sensitive organs for high altitude injury. High-altitude lung diseases include the acute high-altitude lung disease (i.e., high-altitude pulmonary edema), the chronic high-altitude lung disease (i.e., high-altitude pulmonary artery hypertension) and the high-altitude de-adapted reaction. This review summarizes the pathogenic mechanisms and the main therapeutic drugs of high-altitude lung diseases based on the recent research. Moreover, the related formulations and administration routes are also reviewed here. It will provide support and counsel for the diagnosis and treatment of high-altitude lung diseases.

Objective::Regarding the secondary prevention of cardiovascular disease (CVD), there is great interest in preventing recurrent cardiovascular events (RCVEs). The prognostic importance of liver fibrosis scores (LFSs) has previously been reported in various CVDs. We hypothesized that LFSs might also be useful predictors for RCVEs in patients with prior cardiovascular events (CVEs). Herein, we aimed to evaluate the associations of LFSs with RCVEs in a large, real-world cohort of coronary artery disease (CAD) patients with a prior CVE.Methods::In this multicenter prospective study, 6527 consecutive patients with angiography-diagnosed CAD who had experienced a prior CVE (acute coronary syndrome, stroke, percutaneous coronary intervention, or coronary artery bypass grafting) were enrolled. LFSs were computed according to the published formulas: non-alcoholic fatty liver disease fibrosis score (NFS) includes age, body mass index (BMI), impaired fasting glycemia or diabetes mellitus (DM), aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio, platelets, and albumin; fibrosis-4 (FIB-4) includes age, AST, ALT, and platelets; Forns score includes age, gamma-glutamyltransferase (GGT), and platelets; BARD includes BMI, AST/ALT ratio, and DM; GGT/platelet ratio includes GGT and platelets; AST/ALT ratio includes AST and ALT; and AST/platelet ratio index includes AST and platelets. The originally reported cutoffs were used for the categorization of low-, intermediate-, and high-score subgroups. All patients were followed up for the occurrence of RCVEs (comprising cardiovascular death, non-fatal myocardial infarction, and stroke). Cox and Poisson regression analyses were used to assess the relationship of baseline LFSs with the risk of RCVE.Results::During a mean follow-up of (54.67 ± 18.80) months, 532 (8.2%) RCVEs were recorded. Intermediate and high NFS, FIB-4, Forns, and BARD scores were independently associated with an increased risk of RCVE (hazard ratios ranging from 1.42 to 1.75 for intermediate scores and 1.35 to 2.52 for high scores). In the subgroup analyses of sex, age, BMI, DM, and hypertension status, the increased risk of RCVEs with high LFSs (NFS, FIB-4, Forns, and BARD) was maintained across the different subgroups (all P < 0.05). Conclusion::This study showed that LFSs are indeed independently associated with RCVEs, suggesting that LFSs may be used as novel tools for risk stratification in CAD patients with a prior CVE.

Objective::Regarding the secondary prevention of cardiovascular disease (CVD), there is great interest in preventing recurrent cardiovascular events (RCVEs). The prognostic importance of liver fibrosis scores (LFSs) has previously been reported in various CVDs. We hypothesized that LFSs might also be useful predictors for RCVEs in patients with prior cardiovascular events (CVEs). Herein, we aimed to evaluate the associations of LFSs with RCVEs in a large, real-world cohort of coronary artery disease (CAD) patients with a prior CVE.Methods::In this multicenter prospective study, 6527 consecutive patients with angiography-diagnosed CAD who had experienced a prior CVE (acute coronary syndrome, stroke, percutaneous coronary intervention, or coronary artery bypass grafting) were enrolled. LFSs were computed according to the published formulas: non-alcoholic fatty liver disease fibrosis score (NFS) includes age, body mass index (BMI), impaired fasting glycemia or diabetes mellitus (DM), aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio, platelets, and albumin; fibrosis-4 (FIB-4) includes age, AST, ALT, and platelets; Forns score includes age, gamma-glutamyltransferase (GGT), and platelets; BARD includes BMI, AST/ALT ratio, and DM; GGT/platelet ratio includes GGT and platelets; AST/ALT ratio includes AST and ALT; and AST/platelet ratio index includes AST and platelets. The originally reported cutoffs were used for the categorization of low-, intermediate-, and high-score subgroups. All patients were followed up for the occurrence of RCVEs (comprising cardiovascular death, non-fatal myocardial infarction, and stroke). Cox and Poisson regression analyses were used to assess the relationship of baseline LFSs with the risk of RCVE.Results::During a mean follow-up of (54.67 ± 18.80) months, 532 (8.2%) RCVEs were recorded. Intermediate and high NFS, FIB-4, Forns, and BARD scores were independently associated with an increased risk of RCVE (hazard ratios ranging from 1.42 to 1.75 for intermediate scores and 1.35 to 2.52 for high scores). In the subgroup analyses of sex, age, BMI, DM, and hypertension status, the increased risk of RCVEs with high LFSs (NFS, FIB-4, Forns, and BARD) was maintained across the different subgroups (all P < 0.05). Conclusion::This study showed that LFSs are indeed independently associated with RCVEs, suggesting that LFSs may be used as novel tools for risk stratification in CAD patients with a prior CVE.