Endometriosis(EMs)is a common estrogen-depend-ent clinical disease with the pathological characteristics of malig-nant tumors,which has great impact on women's physical and mental health.In recent years,experimental exploration has re-vealed that ectopic foci are in a hypoxic environment outside the uterine cavity,and mitochondria,as the"functional factories"of the cells,play an important role in the process of planting and in-vasion,and the mitochondrial quality control system,which in-cludes mitochondrial oxidative stress,kinetics,autophagy,bio-genesis and calcium homeostasis,is a key mechanism for the e-quilibrium of the mitochondrial function.The mitochondrial quality control system,including mitochondrial oxidative stress kinetics,autophagy,biogenesis and calcium homeostasis,is a key mechanism for mitochondrial functional balance.Therefore,to clarify the role of the mitochondrial quality control system in the development of EMs with the help of rational and rigorous experi-mental and clinical studies can not only help to clarify the patho-genesis of the disease,but also explore the key targets in the prevention and treatment of the disease.Therefore,this article summarizes the research progress of mitochondrial quality control system in endometriosis,with a view to providing reference and theoretical basis for the etiology,pathogenesis and prevention strategies of EMs.

OBJECTIVE To investigate the effects of Chuangling Ye(CLY)on diabetic foot ulcer(DFU)model mice based on the nuclear factor erythroid 2-related factor 2(Nrf2)/solute carrier family 7 member 11(SLC7A11)/glutathione peroxidase 4(GPX4)pathway and explore its potential mechanism.METHODS In animal experiments,streptozotocin(STZ)-induced diabetic mice with full-thickness skin defects were divided into control,model,positive control(recombinant human epidermal growth factor,rhEGF),and CLY low-and high-dose groups(n=10).After 14 days of intervention,wound healing rate was measured.Serum inflammatory factors(IL-6,TNF-α,IL-1β)were detected by ELISA,while oxidative stress markers(SOD,MDA,GSH)and tissue ferrous iron(Fe2+)levels were measured by colorimetric assays.Mitochondrial ultrastructure was observed via transmission electron microscopy(TEM).Nrf2,SLC7A11,and GPX4 expression in wound tissues were analyzed by qPCR and Western blot.In cell experiments,a high glucose(HG)-induced ferroptosis model in human umbilical vein endothelial cells(HUVECs)was established and divided into control,HG,CLY,and CLY combined with pathway inhibitors(ML385,Erastin,RSL3)groups.CCK-8 was used to detect cell via-bility,FerroOrange was used to detect Fe2+content,DCFH-DA and C11-BODIPY 581/591 probes were used to detect intracellular ROS and lipid ROS content,and Western blot was used to detect the expression of proteins such as Nrf2/SLC7A11/GPX4.RESULTS Animal experiments showed that compared with the model group,the wound healing rate in the low-and high-dose CLY groups was significantly improved(P<0.01);the serum IL-6,IL-1β,and TNF-α levels were significantly decreased(P<0.01);the MDA con-tent was significantly reduced(P<0.01),and the SOD activity and GSH content were significantly restored(P<0.05).Colorimetric a-nalysis showed that the low-and high-dose CLY significantly reduced the abnormally elevated Fe2+levels in DFU wounds(P<0.05,P<0.001).Electron microscopy showed that the mitochondrial cristae structure was improved in the low-and high-dose groups.qPCR showed that high-dose CLY upregulated the expression levels of Rno-Nfe2l2(Nrf2),Rno-Slc7a11,Rno-Gpx4,and Rno-Acsl4 mR-NA,and inhibited the expression level of Rno-Acsl4 mRNA(P<0.001).Western blot results showed that CLY upregulated the expres-sion of Nrf2,SLC7A11,GPX4,and FTH1 in DFU wound tissues(P<0.01),while downregulated the level of ACSL4(P<0.01).Cell experiments showed that treatment with CLY increased the survival rate of high glucose-stimulated HUVECs(P<0.001).However,the protective effect of CLY was significantly inhibited after the addition of ML385,Erastin,or RSL3(P<0.01).Treatment with CLY significantly decreased the Fe2+content(P<0.001),which was reversed by ML385,Erastin,or RSL3.The levels of ROS and lipid ROS were also significantly reduced(P<0.001),while the addition of ML385,Erastin,or RSL3 partially weakened the antioxidant effect of CLY.Western blot results showed that CLY significantly upregulated the expression of Nrf2、SLC7A11 and GPX4(P<0.001)and downregulated the expression of 4-HNE and COX2(P<0.01),and ML385,Erastin,or RSL3 could reverse this protective effect.CONCLUSION CLY promotes DFU healing by activating the Nrf2/SLC7A11/GPX4 pathway to inhibit ferroptosis,mitigate oxidative stress,and suppress inflammation,providing a novel therapeutic target for DFU.

Aim To investigate the mechanism by which Aiweixin oral liquid(AWX)alleviates myocar-dial ischemia-reperfusion injury in rats through the reg-ulation of mitochondrial fusion and fission.Methods Seventy-two healthy male Sprague-Dawley rats were randomly assigned to six groups(n=12)using a ran-dom number table:sham surgery group,model group,low-dose AWX(1 mL·kg-1)group,medium-dose AWX(2 mL·kg-1)group,high-dose AWX(4 mL·kg-1)group,and positive control drug trimetazidine(10 mg·kg-1)group.A myocardial ischemia-reper-fusion injury(MIRI)model was established by ligating the left anterior descending coronary artery of the rat heart,followed by 30 minutes of ischemia and 90 mi-nutes of reperfusion.In the sham surgery group,only a suture was placed without ligation.The rats in the treatment groups were pre-gavaged with AWX starting 10 days prior to the modeling procedure.Lead Ⅱ elec-trocardiograms were recorded before and after reperfu-sion in each group to observe the changes in electrocar-diographic parameters.The myocardial infarct size in each group was assessed using TTC staining.The his-topathological changes in myocardial tissue were exam-ined under a light microscope using hematoxylin and eosin(HE)staining.The serum levels of adenosine triphosphate(ATP)and cardiac troponin I(cTnI)were measured using enzyme-linked immunosorbent as-say(ELISA).Superoxide dismutase(SOD)activity and the levels of malondialdehyde(MDA)and lactate dehydrogenase(LDH)were determined using bio-chemical assay kits.The protein expression levels of dynamin-related protein 1(dynamin-relatedprotein 1,DRP1),mitochondrial fission factor(mitochondrial fis-sion factor,MFF),mitochondrial fission protein 1(mi-tochondrial fission protein 1,FIS1),mitofusin 1(mito-fusion-1,MFN1),and mitofusin 2(mitofusion-2,MFN2)were evaluated by Western blot analysis.Re-sults Compared with the sham group,the model group exhibited aggravated myocardial tissue pathological damage,an increased percentage of myocardial infarct size,decreased serum SOD activity and ATP levels,and significantly elevated levels of MDA,cTnI,and LDH activity.Additionally,the protein expression of mito-chondrial fission factors DRP1,MFF,and FIS1 was up-regulated,while the expression of fusion-related factors MFN1 and MFN2 was downregulated.Compared with the model group,Aiweixin oral liquid significantly alle-viated myocardial injury,reduced the percentage of my-ocardial infarct size,increased serum SOD activity and ATP levels,decreased MDA content and cTnI and LDH activity,downregulated the protein expression of mito-chondrial fission factors DRP1,MFF,and FIS1,and up-regulated the protein expression of fusion-related factors MFN1 and MFN2.Conclusion Aiweixin oral liquid alleviates myocardial ischemia-reperfusion injury in rats by regulating abnormal mitochondrial fusion and fis-sion.

Objective To study the damage effect of high-voltage electric shock on skin based on metabolomics,analyze its metabolic differences,and explore its injury mechanism.Methods A total of 16 SPF C57BL/6J male mice were divided into the electric shock group(head skin received electric shock treatment)and control group(head skin received electric shock acoustic-optical stimulation),and the skin appearance after treatment of mice in the two groups was observed.The histopathological changes caused by electric shock were analyzed by HE staining,EVG staining and Masson staining.GC-MS and LC-MS metabonomics were used to analyze the changes of skin metabolism spectrum and tissue metabolites after electric shock exposure,and the differential metabolites were analyzed.The obtained differential metabolites were combined and KEGG enrichment analysis was conducted.Results After high-voltage electric shock,the skin of mice could be damaged to the dermis,and the epidermis was partially thickened,lifted and separated.The structure of skin appendages in the dermis was destroyed,with a large number of inflammatory cells infiltrating and obvious swelling,accompanied by congestion,which led to severe skin inflammatory reaction and impaired skin barrier function.Metabonomics analysis suggested that the metabolites changed after electric shock exposure.KEGG enrichment analysis showed that electric shock significantly affected the central carbon metabolism pathway of cancer,pentose phosphate pathway,purine metabolism,glycine,serine and threonine metabolism processes,amino acid tRNA biosynthesis mechanism,glycerophospholipid metabolism pathway,pyrimidine metabolism pattern,glycolysis/gluconeogenesis,alanine metabolism process,glucagon signal pathway and so on.Conclusion High voltage electric shock can cause deep skin damage,disturb its energy metabolism and amino acid metabolism,and seriously interfere with its antioxidant and DNA repair system functions.

Aim To investigate the mechanism by which Aiweixin oral liquid(AWX)alleviates myocar-dial ischemia-reperfusion injury in rats through the reg-ulation of mitochondrial fusion and fission.Methods Seventy-two healthy male Sprague-Dawley rats were randomly assigned to six groups(n=12)using a ran-dom number table:sham surgery group,model group,low-dose AWX(1 mL·kg-1)group,medium-dose AWX(2 mL·kg-1)group,high-dose AWX(4 mL·kg-1)group,and positive control drug trimetazidine(10 mg·kg-1)group.A myocardial ischemia-reper-fusion injury(MIRI)model was established by ligating the left anterior descending coronary artery of the rat heart,followed by 30 minutes of ischemia and 90 mi-nutes of reperfusion.In the sham surgery group,only a suture was placed without ligation.The rats in the treatment groups were pre-gavaged with AWX starting 10 days prior to the modeling procedure.Lead Ⅱ elec-trocardiograms were recorded before and after reperfu-sion in each group to observe the changes in electrocar-diographic parameters.The myocardial infarct size in each group was assessed using TTC staining.The his-topathological changes in myocardial tissue were exam-ined under a light microscope using hematoxylin and eosin(HE)staining.The serum levels of adenosine triphosphate(ATP)and cardiac troponin I(cTnI)were measured using enzyme-linked immunosorbent as-say(ELISA).Superoxide dismutase(SOD)activity and the levels of malondialdehyde(MDA)and lactate dehydrogenase(LDH)were determined using bio-chemical assay kits.The protein expression levels of dynamin-related protein 1(dynamin-relatedprotein 1,DRP1),mitochondrial fission factor(mitochondrial fis-sion factor,MFF),mitochondrial fission protein 1(mi-tochondrial fission protein 1,FIS1),mitofusin 1(mito-fusion-1,MFN1),and mitofusin 2(mitofusion-2,MFN2)were evaluated by Western blot analysis.Re-sults Compared with the sham group,the model group exhibited aggravated myocardial tissue pathological damage,an increased percentage of myocardial infarct size,decreased serum SOD activity and ATP levels,and significantly elevated levels of MDA,cTnI,and LDH activity.Additionally,the protein expression of mito-chondrial fission factors DRP1,MFF,and FIS1 was up-regulated,while the expression of fusion-related factors MFN1 and MFN2 was downregulated.Compared with the model group,Aiweixin oral liquid significantly alle-viated myocardial injury,reduced the percentage of my-ocardial infarct size,increased serum SOD activity and ATP levels,decreased MDA content and cTnI and LDH activity,downregulated the protein expression of mito-chondrial fission factors DRP1,MFF,and FIS1,and up-regulated the protein expression of fusion-related factors MFN1 and MFN2.Conclusion Aiweixin oral liquid alleviates myocardial ischemia-reperfusion injury in rats by regulating abnormal mitochondrial fusion and fis-sion.

Objective To evaluate the efficacy and safety of transcatheter aortic valve implantation(TAVI)for the treatment of primary aortic valve regurgitation(NAVR)and to compare the difference in the choice of prosthetic valve size and the difference in complications with aortic stenosis(AS).Methods According to the definition of Valve Academic Research Consortium(VARC-3),143 patients with NAVR/AS treated with TAVI and patients with NAVR treated with surgical aortic valve replacement(SAVR)at Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,China,from March 2019 to September 2024 were selected,and clinical data on baseline,perioperative,and primary endpoint events were were retrospectively collected and compared.Results Forty-three patients with NAVR were treated with TAVI,with a device success rate of 86.0％and a surgical success rate of 95.3％.Subgroup comparisons:(1)NAVR-TAVI group than NAVR-SAVR group:patients in the TAVI group had a significantly shorter operative time than those in the SAVR group(P＜0.001);complete left bundle branch block was more likely to occur after TAVI(P=0.042),and complete right bundle branch block was more likely to occur after SAVR(P=0.044).SAVR postoperatively The incidence of congestive heart failure was higher(P=0.013),and the mortality rate was significantly higher in the SAVR group than in the TAVI group(P=0.019).(2)NAVR-TAVI group than AS-TAVI group:the differences in access selection,THV size[28(22,34)mm vs.24(22,32)mm,P=0.044]and proportion of THV overdiameter[14％(7％,20％)vs.7％(3％,11％),P＜0.001]were statistically significant.patients in AS and NAVR groups had 1 case of permanent pacing after TAVI treatment.In the AS and NAVR groups,there was 1 case of permanent pacemaker implantation after TAVI.2 patients in the AS group were converted to surgical treatment,and 6 patients died.Conclusions The use of"off-label"(transfemoral)and"on-label"(transapical)TAVI devices(both from domestic sources)is safer than SAVR for the treatment of NAVR,especially in elderly and high-risk patients.Compared with patients with AS treated with TAVI,larger diameter annulas are usually selected for NAVR,with higher rates of valve migration,but overall safety and efficacy are comparable to AS.

Purpose To investigate the clinical pathological features and treatment strategies of adult pineoblasto-ma(PB).Methods The clinical data of 11 cases of adult PB were retrospectively analyzed.Their imaging,histologi-cal morphology,and immunohistochemical characteristics were evaluated,and the relevant literature was reviewed.Re-sults Among the 11 PB cases,5 cases were female and 6 were male,aged 18-63 years with a median age of 39 years.Microscopically,the tumors were composed of dense small to medium-sized cells,showing a diffuse and sheet-like distribution.Rosette-like structures could be seen in some cases.The tumor cell nuclei were round or irregular with a high nuclear-cytoplasmic ratio.The mitotic figures and apoptosis were extremely common to see,and necrosis was observed in some cases.The tumor cells were uniformly positive for CD56(11/11),Syn(11/11),and CgA(11/11),with retained expression of INI-1(11/11).Some cases were positive for CD99(3/11)and S-100(1/11),while negative for BCOR,CKpan,GFAP,PLAP,CD3,and CD20.The Ki67 proliferation index ranged from 20％to 80％.Five patients were followed up for 2 to 39 months:1 patient developed spinal metastasis 26 months after postop-erative chemotherapy;1 patient had spinal metastasis 4 months after postoperative radiotherapy and temozolomide treat-ment;and 3 patients died.Conclusion PB is a rare,highly malignant tumor in the pineal gland region,even rarer in adults.Its morphology is similar to that of childhood PB,and its prognosis is slightly better than that in children.

Aim To explore the in vitro anti-human triple-negative breast cancer(TNBC)effect and mech-anism of Austocystin R.Methods MTT assay was used to evaluate the anti-tumor potential of Austocystin R for various human tumor cells and normal cells.Flow cytometry was employed to evaluate the influence on cell cycle progression.mRFP-GFP-LC3 adenovirus transfection was used to evaluate the autophagic flux process.Western blot assay was used to verify the effect of Austocystin R on the expression of related pro-teins.Results The results showed that Austocystin R significantly inhibited the proliferation of multiple tumor cells in a dose-dependent manner,especially for the MDA-MB-231 cells with an IC50 of 1.45μmol·L-1.In addition,Austocystin R increased the protein expression of PTEN,p53,p-p53,p27,p21,and down-regulated the expression of p-PI3K,p-AKT and p-mTOR.Austocystin R can significantly increase the proportion of S-phase MDA-MB-231 cells,inhibit the expression of Cyclin D1,CDK4,CDK6,Rb,Cyclin B1 and CDK1,and promote the expression of Cyclin E1 and CDK2.Austocystin R can promote the autophagic flux process of MDA-MB-231 cells,promote the expres-sion of LC3 Ⅰ/Ⅱ,p-Beclin-1,p-ULK1,HMGB-1 and Atg 14 proteins,and inhibit the expression of Beclin-1,ULK1,p62,ATG 3,ATG 4B,ATG 5,ATG 7,ATG 12,ATG 13 and ATG 16L1 proteins.Conclusion Austo-cystin R can exhibit its anti-TNBC activity by inhibi-ting the PI3K/AKT/mTOR signaling pathway,blocking the cell cycle at the S phase and inducing autophagic cell death.

Purpose To investigate the clinical pathological features and treatment strategies of adult pineoblasto-ma(PB).Methods The clinical data of 11 cases of adult PB were retrospectively analyzed.Their imaging,histologi-cal morphology,and immunohistochemical characteristics were evaluated,and the relevant literature was reviewed.Re-sults Among the 11 PB cases,5 cases were female and 6 were male,aged 18-63 years with a median age of 39 years.Microscopically,the tumors were composed of dense small to medium-sized cells,showing a diffuse and sheet-like distribution.Rosette-like structures could be seen in some cases.The tumor cell nuclei were round or irregular with a high nuclear-cytoplasmic ratio.The mitotic figures and apoptosis were extremely common to see,and necrosis was observed in some cases.The tumor cells were uniformly positive for CD56(11/11),Syn(11/11),and CgA(11/11),with retained expression of INI-1(11/11).Some cases were positive for CD99(3/11)and S-100(1/11),while negative for BCOR,CKpan,GFAP,PLAP,CD3,and CD20.The Ki67 proliferation index ranged from 20％to 80％.Five patients were followed up for 2 to 39 months:1 patient developed spinal metastasis 26 months after postop-erative chemotherapy;1 patient had spinal metastasis 4 months after postoperative radiotherapy and temozolomide treat-ment;and 3 patients died.Conclusion PB is a rare,highly malignant tumor in the pineal gland region,even rarer in adults.Its morphology is similar to that of childhood PB,and its prognosis is slightly better than that in children.

Aim To explore the in vitro anti-human triple-negative breast cancer(TNBC)effect and mech-anism of Austocystin R.Methods MTT assay was used to evaluate the anti-tumor potential of Austocystin R for various human tumor cells and normal cells.Flow cytometry was employed to evaluate the influence on cell cycle progression.mRFP-GFP-LC3 adenovirus transfection was used to evaluate the autophagic flux process.Western blot assay was used to verify the effect of Austocystin R on the expression of related pro-teins.Results The results showed that Austocystin R significantly inhibited the proliferation of multiple tumor cells in a dose-dependent manner,especially for the MDA-MB-231 cells with an IC50 of 1.45μmol·L-1.In addition,Austocystin R increased the protein expression of PTEN,p53,p-p53,p27,p21,and down-regulated the expression of p-PI3K,p-AKT and p-mTOR.Austocystin R can significantly increase the proportion of S-phase MDA-MB-231 cells,inhibit the expression of Cyclin D1,CDK4,CDK6,Rb,Cyclin B1 and CDK1,and promote the expression of Cyclin E1 and CDK2.Austocystin R can promote the autophagic flux process of MDA-MB-231 cells,promote the expres-sion of LC3 Ⅰ/Ⅱ,p-Beclin-1,p-ULK1,HMGB-1 and Atg 14 proteins,and inhibit the expression of Beclin-1,ULK1,p62,ATG 3,ATG 4B,ATG 5,ATG 7,ATG 12,ATG 13 and ATG 16L1 proteins.Conclusion Austo-cystin R can exhibit its anti-TNBC activity by inhibi-ting the PI3K/AKT/mTOR signaling pathway,blocking the cell cycle at the S phase and inducing autophagic cell death.