Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences最新文献

{"title":"[Knockdown of nuclear protein 1 delays pathological pro-gression of osteoarthritis through inhibiting chondrocyte ferroptosis].","authors":"Taiyang Liao, Zhenyuan Ma, Deren Liu, Lei Shi, Jun Mao, Peimin Wang, Liang Ding","doi":"10.3724/zdxbyxb-2024-0091","DOIUrl":"10.3724/zdxbyxb-2024-0091","url":null,"abstract":"<p><strong>Objectives: </strong>To investigate the effect of nuclear protein (Nupr) 1 on the pathological progression of osteoarthritis and its relationship with ferroptosis of chondrocytes.</p><p><strong>Methods: </strong>Chondrocytes from mouse knees were divided into small interfering RNA (siRNA) control group, small interfering RNA targeting Nupr1 (siNupr1) group, siRNA control+IL-1β group (siRNA control interference for 24 h followed by 10 ng/mL IL-1β) and siNupr1+IL-1β group (siNupr1 interference for 24 h followed by 10 ng/mL IL-1β). The protein and mRNA expressions of Nupr1 were detected by Western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR). Cell proliferation viabilities were measured using the cell counting kit-8 method. The levels of ferrous ions were detected by FerroOrange staining. Lipid peroxidation levels were detected by C11-BODIPY-591 fluorescence imaging. The contents of malondialdehyde (MDA) and glutathione (GSH) were detected by enzyme-linked immunosorbent assay. The protein expressions of acyl-CoA synthetase long-chain family (ACSL) 4, P53, glutathione peroxidase (GPX) 4 and solute carrier family 7 member 11 gene (SLC7A11) were detected by Western blotting. The osteoarthritis model was constructed by destabilization of the medial meniscus (DMM) surgery in 7-week-old male C57BL/6J mice. The mice were randomly divided into four groups with 10 animals in each group: sham surgery (Sham)+adeno-associated virus serotype 5 (AAV5)-short hairpin RNA (shRNA) control group, Sham+AAV5-shRNA control targeting <i>Nupr1</i> (shNupr1) group, DMM+AAV5-shRNA control group, and DMM+AAV5-shNupr1 group. Hematoxylin and eosin staining and Safranin O-Fast Green staining were used to observe the morphological changes in cartilage tissue. The Osteoarthritis Research Society International (OARSI) osteoarthritis cartilage histopathology assessment system was used to evaluate the degree of cartilage degeneration in mice. The mRNA expressions of matrix metallopeptidase (MMP) 13, a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) 5, cyclooxy-genase (COX) 2, and GPX4 were detected by qRT-PCR.</p><p><strong>Results: </strong><i>In vitro</i> experiments showed that knocking down <i>Nupr1</i> alleviated the decrease of chondrocyte proliferation activity induced by IL-1β, reduced iron accumulation in mouse chondrocytes, lowered lipid peroxidation, downregulated ACSL4 and P53 protein expression and upregulated GPX4 and SLC7A11 protein expression (all <i>P</i><0.01), thereby inhibiting ferroptosis in mouse chondrocytes. Meanwhile, <i>in vivo</i> animal experiments demonstrated that knocking down <i>Nupr1</i> delayed the degeneration of articular cartilage in osteoarthritis mice, improved the OARSI score, slowed down the degradation of the extracellular matrix in osteoarthritis cartilage, and reduced the expression of the key ferroptosis regulator GPX4 (all <i>P</i><0.01).</p><p><strong>Conclusions: </","PeriodicalId":24007,"journal":{"name":"Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences","volume":" ","pages":"669-679"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736347/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142558978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Research progress on the role of ferroptosis in aortic dissection].","authors":"Xiang Hong, Yuchong Zhang, Weiguo Fu, Lixin Wang","doi":"10.3724/zdxbyxb-2024-0186","DOIUrl":"10.3724/zdxbyxb-2024-0186","url":null,"abstract":"<p><p>Recent studies have shown that iron metabolism dysregulation and lipid peroxidation-induced ferroptosis, triggered by oxidative stress, play a key role in the development of aortic dissection. Dysregulated iron metabolism leads to excessive production of hydroxyl radicals due to abnormal iron levels and heme metabolism, while lipid peroxidation is linked to system Xc^－ dysfunction and accumulation of phospholipid hydroperoxides. These factors synergistically disrupt aortic homeostasis and drive ferroptosis in vascular cells, including endothelial and smooth muscle cells. Furthermore, disruptions in ferroptosis-related genes, along with risk factors such as smoking, epigenetic modifications such as protein methylation, and abnormalities in immune cells, particularly T cells, are closely linked to aortic dissection. Several small molecules and nanomaterials have shown potential in inhibiting ferroptosis in this context. This review elucidates the roles of ferroptosis in aortic dissection and proposes strategies for its targeted prevention and treatment.</p>","PeriodicalId":24007,"journal":{"name":"Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences","volume":" ","pages":"726-734"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736346/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142855806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Preparation of decellularized bone graft material with supercritical carbon dioxide extraction technique].","authors":"Feng Hao, Kaifeng Pan, Liuyun Huang, Xuhong Chen, Haikun Wei, Xianhua Chen, Jianfeng Zhang","doi":"10.3724/zdxbyxb-2024-0108","DOIUrl":"10.3724/zdxbyxb-2024-0108","url":null,"abstract":"<p><strong>Objectives: </strong>To evaluate the immunogenicity and osteogenic ability of animal-derived bone graft material decellularized with supercritical carbon dioxide.</p><p><strong>Methods: </strong>Porcine femurs were randomly divided into two groups after preliminary treatment, and decellularized with conventional method (control group) or supercritical carbon dioxide (experimental group). Allogenic demineralized bone matrix was used as positive control. Clearance rate of galactose-α-1, 3-galactose (α-Gal) antigen was determined by enzyme-linked immunosorbent assay and residual DNA was detected by a fluorescence method. Nine SPF-grade male athymic nude mice of 6 weeks old were randomly divided into experimental, control and positive control groups. Samples were implanted over biceps femoris muscle of athymic nude mice. The explants were collected 4 weeks post implantation. Hematoxylin and eosin (HE) staining and immunohistochemistry were applied to determine the osteogenic ability and bone tissue-associated protein expressions of the implants.</p><p><strong>Results: </strong>The clearance rates of α-Gal antigen in the experimental group and the control group were (99.09±0.26)% and (30.18±2.02)%, respectively (<i>t</i>=58.67, <i>P<</i>0.01). The residual DNA of the experimental, control and positive control groups were (13.49±0.07), (15.20±0.21) and (14.70±0.17) ng/mg. The residual DNA in the experimental group was significantly lower than that in the control group (<i>t</i>=－13.41, <i>P</i><0.01) and positive control group (<i>t</i>=－11.30, <i>P</i><0.01). HE staining results showed that multiple bone formation centers with active osteogenesis and rich bone marrow were observed in experimental group 4 weeks after implantation, but only a small number of bone formation centers were observed in the control and positive control groups, with no obvious osteoblasts present. Immunohistochemistry results indicated that the expressions of alkaline phosphatase, Runt-related transcription factor 2, collagen typeⅠand osteocalcin in the experimental group showed an increasing trend compared with those in the control and positive control groups.</p><p><strong>Conclusions: </strong>Compared with clinically used allogenic demineralized bone matrix and bone graft material decellularized with conventional method, bone graft material decellularized with supercritical carbon dioxide exhibits lower immunogenicity and better osteogenic ability.</p>","PeriodicalId":24007,"journal":{"name":"Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences","volume":" ","pages":"772-778"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142558979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Inhibition of miR-30d-5p promotes mitochondrial autophagy and alleviates high glucose-induced injury in podocytes].","authors":"Ying Cai, Sheng Chen, Xiaoli Jiang, Qiyuan Wu, Bei Guo, Fang Wang","doi":"10.3724/zdxbyxb-2024-0504","DOIUrl":"10.3724/zdxbyxb-2024-0504","url":null,"abstract":"<p><strong>Objectives: </strong>To study the role of microRNA (miR)-30d-5p in high glucose-induced podocyte injury.</p><p><strong>Methods: </strong>Podocytes were hyperglycated with 30 mmol/L glucose, transfected with miR-30d-5p inhibitor and mimic, and then treated with 1 mg/mL 3-methyladenine (3-MA). The transfection efficiency of miR-30d-5p was quantified by reverse transcription PCR. Apoptosis was detected by flow cytometry. The expressions of nephrin, microtubule-associated protein light chain (LC) 3Ⅱ/LC3Ⅰ, P62, autophagy-related gene (ATG) 5, PTEN induced putative kinase (PINK) 1 and Parkin gene (PARK2) were detected by Western blotting. The mito-chondrial membrane potential was detected by JC-1 fluorescent probe, and adenosine triphosphate (ATP) content in cells was detected by relevant kits.</p><p><strong>Results: </strong>Under high glucose induction, podocyte apoptosis increased, miR-30d-5p and P62 expressions were upregulated, while nephrin, ATG5, PINK1, PARK2 and LC3Ⅱ/LC3Ⅰ expressions decreased (all <i>P</i><0.01). MiR-30d-5p inhibitor reversed the effect of high glucose on apoptosis, and the expression of ATG5, PINK1, PARK2, nephrin, LC3Ⅱ/LC3Ⅰ and P62 (all <i>P</i><0.01). High glucose induced loss of mitochondrial membrane potential and ATP content in podocytes, while inhibition of miR-30d-5p increased them. Autophagy inhibitors 3-MA and miR-30d-5p mimics reversed the effects of miR-30d-5p inhibition on apoptosis, autophagy and mitochondrial function of podocytes induced by high glucose (all <i>P</i><0.05).</p><p><strong>Conclusions: </strong>Inhibition of miR-30d-5p may promote mitochondrial autophagy (mitophagy) by promoting the expression of ATG5, PINK1, PARK2 and alleviating high glucose-induced podocyte damage.</p>","PeriodicalId":24007,"journal":{"name":"Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences","volume":" ","pages":"756-764"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736342/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142819203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Protective environment strategies for hematopoietic stem cell transplantation: progress and prospects].","authors":"Xiaoyu Zhou, Jianli Zhang, Liwei Xu, Aiyun Jin","doi":"10.3724/zdxbyxb-2024-0082","DOIUrl":"10.3724/zdxbyxb-2024-0082","url":null,"abstract":"<p><p>With the progress of hematopoietic stem cell transplantation technology, the reduction of pretreatment intensity, the shortening of bone marrow suppression time and the reduction of infection risk, especially the physical and psychological stress for doctors and patients caused by rigorous protection procedures, the protective environment strategies need improvement. It has been found that, regardless of whether total environment protection is implemented, there is no significant difference in the outcomes of chemotherapy patients with neutropenia. Therefore, the traditional protective environment strategies are being improved. The protective environment strategies for hematopoietic stem cell transplantation patients have developed rapidly in the past two decades, from the replacement of laminar flow equipment by high-efficiency filtration devices to the development of home care after transplantation. In this article, the progress in protective environment strategies for hematopoietic stem cell transplantation patients is reviewed and further reflect, providing reference for future improvement.</p>","PeriodicalId":24007,"journal":{"name":"Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences","volume":" ","pages":"796-803"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736351/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142795319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Causal relationship between ferroptosis-related gene HSPA5 and hepatocellular carcinoma: a study based on mendelian randomization and mediation analysis].","authors":"Bing Cui, Chengcheng Xu, Yuan Xu, Aqin Chen, Chaoming Mao, Yuehua Chen","doi":"10.3724/zdxbyxb-2024-0095","DOIUrl":"10.3724/zdxbyxb-2024-0095","url":null,"abstract":"<p><strong>Objectives: </strong>To explore a causal relationship between ferroptosis-related gene heat shock protein A5 (HSPA5) and hepatocellular carcinoma (HCC).</p><p><strong>Methods: </strong>A two-sample Mendelian randomization (MR) design was employed to evaluate the causal relationships among HSPA5, regulatory T cells (Tregs), and HCC. Single nucleotide polymorphisms (SNPs) associated with HSPA5, Tregs and HCC were selected as instrumental variables through publicly available genome-wide association studies (GWAS) databases. MR analysis was used to assess the direct effect of HSPA5 on HCC, followed by two-step MR to analyze the potential mediating role of Tregs. Reverse MR analysis was conducted with HCC as the exposure and HSPA5 as the outcome. Inverse variance weighting was the primary method for testing causal associations in all MR analyses. Robustness of the results was confirmed through MR-Egger, weighted median, weighted mode, and simple mode methods. Heterogeneity of instrumental variables was evaluated using Cochrane's <i>Q</i> statistic, while pleiotropy was tested by MR-Egger intercept and MR-PRESSO, with leave-one-out sensitivity analysis performed for robustness. Data from The Cancer Genome Atlas (TCGA) and Human Protein Atlas (HPA) were utilized to verify the expression levels of HSPA5 in HCC tissues and its correlation with Tregs to reveal the interaction mechanisms between HSPA5 and Tregs in HCC progression and their relationship with patient prognosis.</p><p><strong>Results: </strong>MR analysis showed a positive correlation between elevated HSPA5 expression and HCC risk (all <i>P</i><0.01), while reverse MR analysis found no statistically significant association between HCC and HSPA5 (<i>P</i>>0.05). HSPA5 expression was significantly correlated with Tregs function (all <i>P</i><0.05), and the enrichment of Tregs in HCC microenvironment was positively associated with HCC progression (all <i>P</i><0.05). Mediation analysis indicated that Tregs accounted for 5.00% and 7.45% of the mediation effect between HSPA5 and HCC. TCGA and HPA database analysis revealed that both HSPA5 mRNA and protein expression levels were higher in HCC tissues compared to normal tissues, and high HSPA5 expression was significantly associated with poor prognosis. Immune infiltration analysis confirmed a significant positive correlation between HSPA5 and Tregs, with high Tregs infiltration closely related to HCC progression.</p><p><strong>Conclusions: </strong>Elevated HSPA5 expression is significantly associated with HCC development and poor prognosis. HSPA5 may promote HCC progression by regulating the function of Tregs in the tumor microenvironment.</p>","PeriodicalId":24007,"journal":{"name":"Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences","volume":" ","pages":"691-698"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736341/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142629491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Ferroptosis-related genes in osteoporosis: a bioinformatics analysis and <i>in vitro</i> study].","authors":"Yushuang Xia, Bo Wang, Pengfei Pan, Xiangshun Ren, Lixi Gao, Jian Xiong, Yan Ma","doi":"10.3724/zdxbyxb-2024-0089","DOIUrl":"10.3724/zdxbyxb-2024-0089","url":null,"abstract":"<p><strong>Objectives: </strong>To explore ferroptosis-related genes in osteoporosis through bioinformatic analysis and <i>in vitro</i> study.</p><p><strong>Methods: </strong>Osteoporosis-related genes were identified from dataset GSE35958 in the Gene Expression Omnibus database; and the ferroptosis-related genes were identified from the FerrDb database. These were intersected with the differentially expressed genes in GSE35958 to obtain ferroptosis-related genes in osteoporosis. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed for the differentially expressed genes. And Spearman correlation and protein-protein interaction network analysis were performed. Then, the hub genes of ferroptosis in osteoporosis were screened by Degree, MNC, EPC, MCC and DMNC in Cytoscape software CytoHubba plugin; and analyzed with receiver operating characteristic (ROC) curves. The bone marrow mesenchymal stem cells from osteoporosis patients (osteoporosis group) and non-osteoporosis patients (control group) were subjected to quantitative reverse transcription polymerase chain reaction to detect the messenger RNA expression of ferroptosis hub genes in both groups.</p><p><strong>Results: </strong>A total of 32 differentially expressed genes related to ferroptosis in osteoporosis were identified, including 26 up-regulated genes and 6 down-regulated genes. GO enrichment analysis showed that the identified genes were mainly involved in intercellular adhesion, lipid metabolism and cytokine response. KEGG enrichment analysis showed that the genes were mainly involved in signaling pathways of adhesive plaques, MAPK, PI3K-Akt, and Wnt. Spearman correlation analysis showed correlation among differentially expressed genes. Six hub genes for ferroptosis in osteoporosis were obtained, namely <i>MAPK3</i>, <i>CDKN1A</i>, <i>MAP1LC3A</i>, <i>TNF</i>, <i>RELA</i>, and <i>TGF</i>-<i>β1</i>. ROC curve analysis showed that these hub genes had good diagnostic performance in osteoporosis and may become potential biomarkers of osteoporosis. <i>In vitro</i> experiments confirmed significant differences in these hub genes between the control group and the osteoporosis group (all <i>P</i><0.05).</p><p><strong>Conclusions: </strong>This study has identified six ferroptosis-related hub genes in osteoporosis, which may be used as novel biomarkers for the early diagnosis and treatment of osteoporosis.</p>","PeriodicalId":24007,"journal":{"name":"Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences","volume":" ","pages":"680-690"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736348/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142750644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Clinical significance of tertiary lymphoid structure maturity in colorectal cancer patients].","authors":"Jiangjiang Zheng, Jingjing Yu, Jingjing Xie, Dong Chen, Hong Deng","doi":"10.3724/zdxbyxb-2024-0320","DOIUrl":"10.3724/zdxbyxb-2024-0320","url":null,"abstract":"<p><strong>Objectives: </strong>To explore the clinical significance of the tertiary lymphoid structure (TLS) maturity in colorectal cancer patients.</p><p><strong>Methods: </strong>A total of 230 surgically removed colorectal cancer specimens with detailed follow-up data were collected from Yinzhou Second Hospital. The patients were divided into mature TLS group and immature TLS group according to immunohistochemical results. The patient age, gender, maximum tumor diameter, tumor location, differentiation degree, depth of invasion, lymph node metastasis, vascular tumor thrombus, liver metastasis, distant non-liver metastasis, mismatch repair status, expression of Ki-67, P53 and programmed death-ligand (PD-L) 1 were analyzed. The Kaplan-Meier method (Breslow test) was used to analyze the survival of patients, and multivariate Cox regression model was applied to analyze the prognostic factors.</p><p><strong>Results: </strong>There were 128 cases of mature TLS and 102 cases of immature TLS. Compared to the immature TLS group, the mature TLS group showed a significantly lower rate of vascular tumor thrombus, lymph node metastasis, and liver metastasis. Additionally, the positive expression rate of Ki-67 was markedly reduced, while the rate of deficient mismatch repair and the positive rate of PD-L1 were significantly increased (all <i>P</i><0.05). The overall survival rate of the mature TLS group was superior to that of the immature TLS group (Breslow=4.553, <i>P</i><0.05). Cox regression analysis indicated that lymph node metastasis was an independent risk factor for the prognosis of colorectal cancer patients (<i>P</i><0.01), while TLS maturation was a protective factor (<i>P</i><0.05).</p><p><strong>Conclusions: </strong>The formation of TLS may play a significant role in inhibiting lymph node metastasis, liver metastasis, and vascular tumor thrombus in colorectal cancer. In addition, patients with mature TLS have a favorable clinical prognosis.</p>","PeriodicalId":24007,"journal":{"name":"Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences","volume":" ","pages":"765-771"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142772941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Myeloid-derived suppressor cells as important factors and potential targets for breast cancer progression].","authors":"Nannan DU, Hua Wan, Hailing Guo, Xukuan Zhang, Xueqing Wu","doi":"10.3724/zdxbyxb-2024-0353","DOIUrl":"10.3724/zdxbyxb-2024-0353","url":null,"abstract":"<p><p>Recurrence and metastasis remain the leading cause of death in breast cancer patients due to the lack of effective treatment. A microenvironment suitable for cancer cell growth, referred to as pre-metastatic niche (PMN), is formed in distant organs before metastasis occurs. Myeloid-derived suppressor cells (MDSCs) are a heterogenous population of immature myeloid cells with immunosuppressive effects. They can expand in large numbers in breast cancer patients and participate in the formation of PMN. MDSCs can remodel the extracellular matrix of pulmonary vascular endothelial cells and recruit cancer stem cells to promote the lung metastasis of breast cancer. Furthermore, MDSCs facilitate immune evasion of breast cancer cells to impact the efficacy of immunotherapy. It is proposed that MDSCs represent a potential therapeutic target for the inhibition of recurrence and metastasis in breast cancer. Therapeutic strategies targeting MDSCs have shown promising efficacy in preclinical studies and clinical trials. This review presents a summary of the principal factors involved in the recruitment and activation of MDSCs during the formation of PMN, and outlines MDSCs functions such as immunosuppression and the current targeted therapies against MDSCs, aiming to provide new ideas for the treatment of distant metastases in breast cancer.</p>","PeriodicalId":24007,"journal":{"name":"Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences","volume":" ","pages":"785-795"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736353/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142839807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Roles of ferroptosis in the development of diabetic nephropathy].","authors":"Pan Liu, Zhengdong Zhang, Qiu Chen","doi":"10.3724/zdxbyxb-2024-0114","DOIUrl":"10.3724/zdxbyxb-2024-0114","url":null,"abstract":"<p><p>Diabetic nephropathy is a common microvascular complication of diabetes mellitus and one of the main causes of death in patients with diabetes mellitus. Ferroptosis is a newly discovered iron-dependent regulated cell death, which may contribute to the pathogenesis and development of diabetic nephropathy. Adenosine monophosphate-activated protein kinase (AMPK)-mediated ferroptosis-related signaling pathways can slow down the progression of diabetic nephropathy, but excessive activation of AMPK signaling pathway may induce cells to undergo autophagic death. Activation of the signaling pathway mediated by nuclear factor-erythroid 2-related factor (Nrf) 2 and heme oxygenase (HO)-1 can inhibit ferroptosis of cells and alleviate diabetic nephropathy. However, the regulatory effect of HO-1 on ferroptosis is bidirectional, and activation of HIF-1α/HO-1 pathway may lead to intracellular iron overload and ultimately promote ferroptosis. Transforming growth factor (TGF)-β1 mediated signaling pathways can accelerate lipid peroxidation by down-regulating the levels of SLC7A11/GSH/GPX4. The ferroptosis-related signaling pathways mediated by exosome lncRNAs/circRNAs/miRNAs are also involved in the pathogenesis and development of diabetic nephropathy. In addition, signaling pathways mediated by stimulator of interferon gene (STING) and the novel ferroptosis promoter acyl-CoA synthetase long-chain family (ACSL) 1 can induce ferroptosis to promote the progression of diabetic nephropathy. In this review, we focus on the roles of ferroptosis in diabetic nephropathy through the signaling pathways mediated by AMPK, Nrf2/HO-1, TGF-β and exosomes, to elaborate the pathogenesis and development of diabetic nephropathy, and the potential therapeutic target for diabetic nephropathy.</p>","PeriodicalId":24007,"journal":{"name":"Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences","volume":"53 6","pages":"708-714"},"PeriodicalIF":0.0,"publicationDate":"2024-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11736350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142932929","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}