Experimental and therapeutic medicine最新文献

{"title":"FRZB affects <i>Staphylococcus</i> aureus‑induced osteomyelitis in human bone marrow derived stem cells by regulating the Wnt/β‑catenin signaling pathway.","authors":"Xin Li,&nbsp;Wenyong Pang,&nbsp;Hongsong Fan,&nbsp;Hao Wang,&nbsp;Leibing Zhang","doi":"10.3892/etm.2023.12230","DOIUrl":"10.3892/etm.2023.12230","url":null,"abstract":"<p><p>Osteomyelitis is an infectious disease of bone tissue caused by bacterial infection, which can infect through hematogenous, traumatic or secondary ways and then lead to acute or chronic bone injury and relative clinical symptoms, bringing physical injury and economic burden to patients. Frizzled related protein (FRZB) participates in the regulation of various diseases (osteoarthritis, cardiovascular diseases and types of cancer) by regulating cell proliferation, motility, differentiation and inflammation, while its function in osteomyelitis remains to be elucidated. The present study aimed to uncover the role and underlying mechanism of FRZB mediation in <i>Staphylococcus aureus</i> (<i>S. aureus</i>)-induced osteomyelitis. Human bone marrow derived stem cells (hBMSCs) were treated with <i>S. aureus</i> to imitate an inflammatory osteomyelitis micro-environment <i>in vitro</i>, then mRNA and protein expression were severally assessed by RT-PCR and western blotting. The activity, apoptosis and differentiation of the cells were characterized via CCK-8, caspase-3 activity and Alizarin red sulfate/alkaline phosphatase staining, respectively. Expression levels of FRZB were upregulated in <i>S</i>. <i>aureus</i>-infected hBMSCs. Over-expression of FRZB significantly reduced hBMSC cell viability and differentiation while promoting cell apoptosis with or without <i>S</i>. <i>aureus</i> infection. However, FRZB knockdown reversed these effects. Once Wnt was impeded, the effect of FRZB downregulation was impeded to a great extent. Taken together, FRZB participated to regulate the osteomyelitis by activating the Wnt/β-catenin signaling pathway.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"26 5","pages":"531"},"PeriodicalIF":0.0,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/2f/87/etm-26-05-12230.PMC10587868.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49695420","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":"Role of dysregulated ferroptosis‑related genes in cardiomyocyte ischemia‑reperfusion injury: Experimental verification and bioinformatics analysis.","authors":"Tie Hu,&nbsp;Wen-Peng Yu,&nbsp;Hua-Xi Zou,&nbsp;Zhi-Hao Chai,&nbsp;Shu-Yu Le,&nbsp;Fa-Jia Hu,&nbsp;Yi-Cheng Wang,&nbsp;Huang Huang,&nbsp;Song-Qing Lai,&nbsp;Ji-Chun Liu","doi":"10.3892/etm.2023.12233","DOIUrl":"10.3892/etm.2023.12233","url":null,"abstract":"<p><p>Acute myocardial infarction is a life-threatening condition with high mortality and complication rates. Although myocardial reperfusion can preserve ischemic myocardial tissue, it frequently exacerbates tissue injury, a phenomenon known as ischemia-reperfusion injury (IRI). However, the underlying pathological mechanisms of IRI remain to be completely understood. Ferroptosis is a novel type of regulated cell death that is associated with various pathological conditions, including angiocardiopathy. The purpose of this article was to elucidate the possible mechanistic role of ferroptosis in IRI through bioinformatics analysis and experimental validation. Healthy and IRI heart samples were screened for differentially expressed ferroptosis-related genes and functional enrichment analysis was performed to determine the potential crosstalk and pathways involved. A protein-protein interaction network was established for IRI, and 10 hub genes that regulate ferroptosis, including <i>HIF1A</i>, <i>EGFR</i>, <i>HMOX1</i>, and <i>ATF3</i> were identified. <i>In</i> vitro, an anoxia/reoxygenation (A/R) injury model was established using H9c2 cardiomyoblasts to validate the bioinformatics analysis results, and extensive ferroptosis was detected. A total of 4 key hub genes and 3 key miRNAs were also validated. It was found that IRI was related to the aberrant infiltration of immune cells and the small-molecule drugs that may protect against IRI by preventing ferroptosis were identified. These results provide novel insights into the role of ferroptosis in IRI, which can help identify novel therapeutic targets.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"26 5","pages":"534"},"PeriodicalIF":0.0,"publicationDate":"2023-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fb/81/etm-26-05-12233.PMC10587876.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49695424","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":"Metformin regulates the LIN28B‑mediated JNK/STAT3 signaling pathway through miR‑140‑3p in subretinal fibrosis.","authors":"Zhijuan Hua,&nbsp;Wenchang Yang,&nbsp;Dongli Li,&nbsp;Yixin Cui,&nbsp;Lu Shen,&nbsp;Lingna Rao,&nbsp;Yuxiang Zheng,&nbsp;Qiying Zhang,&nbsp;Wenyi Zeng,&nbsp;Yi Gong,&nbsp;Ling Yuan","doi":"10.3892/etm.2023.12227","DOIUrl":"10.3892/etm.2023.12227","url":null,"abstract":"<p><p>Subretinal fibrosis (SF) is an important cause of submacular neovascularization that leads to permanent vision loss, but has no effective clinical treatment. The present study examined the influence of metformin on SF, and investigated whether the mechanism involves the microRNA (miR)-140-3p/LIN28B/JNK/STAT3-mediated regulation of oxidative stress, angiogenesis and fibrosis-associated indicators. A mouse model of laser-induced SF was established. In addition, an ARPE-19 fibrotic cell model was established using TGF-β1. A Cell Counting Kit-8 assay was used to examine cell viability. Flow cytometry was used to measure reactive oxygen species levels, and western blotting was used to detect the levels of proteins associated with epithelial-mesenchymal transition (EMT), signaling and fibrosis. The levels of superoxide dismutase, malondialdehyde, glutathione-peroxidase and catalase were measured using kits. Scratch assays and Transwell assays were used to assess cell migration and invasion, respectively, and reverse transcription-quantitative PCR was used to determine the levels of miR-140-3p and LIN28B. Dual-luciferase assays were used to verify the targeting relationship between miR-140-3p and LIN28B, and coimmunoprecipitation was used to confirm the interaction between LIN28B and JNK. Masson staining and hematoxylin and eosin staining were used to examine collagenous fibers and the histopathology of eye tissue. In ARPE-19 cells induced by TGF-β1, metformin promoted miR-140-3p expression and inhibited LIN28B expression and JNK/STAT3 pathway activation, thereby inhibiting oxidative stress, EMT and fibrosis in ARPE-19 cells. The overexpression of LIN28B or treatment with the JNK/STAT3 agonist anisomycin partially reversed the inhibitory effect of metformin on oxidative stress and fibrosis in ARPE-19 cells. The dual-luciferase reporter assay and coimmunoprecipitation assay showed that miR-140-3p targeted the 3' untranslated region of LIN28B mRNA and inhibited LIN28B expression. LIN28B targeted and bound to JNK and regulated the JNK/STAT3 pathway. Therefore, it may be concluded that metformin can promote miR-140-3p expression, inhibit LIN28B and then inhibit the JNK/STAT3 pathway to alleviate SF.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"26 5","pages":"528"},"PeriodicalIF":0.0,"publicationDate":"2023-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/57/f9/etm-26-05-12227.PMC10587880.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49695423","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":"Salsolinol improves angiotensin II‑induced myocardial fibrosis <i>in vitro</i> via inhibition of LSD1 through regulation of the STAT3/Notch‑1 signaling pathway.","authors":"Xian Zhang,&nbsp;Ze Shao,&nbsp;Yuchao Ni,&nbsp;Feilong Chen,&nbsp;Xia Yu,&nbsp;Jiasheng Wen","doi":"10.3892/etm.2023.12226","DOIUrl":"10.3892/etm.2023.12226","url":null,"abstract":"<p><p>The clinical incidence of congestive heart failure (CHF) is very high and it poses a significant threat to the health of patients. The traditional Chinese medicine monomer salsolinol is widely used to treat similar symptoms of CHF. However, there have been no reports on the effect of salsolinol for the management of CHF and its effects on myocardial fibrosis. In the present study, salsolinol was used to treat angiotensin II (AngII)-induced human cardiac fibroblasts (HCFs) and cell proliferation and migration were assessed using a CCK-8, EdU staining assay and wound healing assay. Subsequently, immunofluorescence, western blotting and other techniques were used to detect indicators associated with cell fibrosis and relevant kits were used to detect markers of cellular inflammation and reactive oxygen species (ROS) production. Molecular docking analysis was used to predict the relationship between salsolinol and lysine-specific histone demethylase 1A (LSD1). Subsequently, the expression of LSD1 in the serum of CHF patients was detected by reverse transcription-quantitative PCR. Finally, LSD1 was overexpressed in cells to explore the regulatory mechanism of salsolinol in AngII-induced HFCs. Salsolinol reduced the proliferation and migration. Salsolinol reduced the expression of fibrosis marker proteins α-smooth muscle actin, Collagen I and Collagen III in a concentration-dependent manner, thereby reducing cell fibrosis. In addition, salsolinol reduced the levels of TNF-α and IL-6 in the cell supernatant and ROS production following AngII induction. Salsolinol inhibited LSD1 expression and regulated the STAT3/Notch-1 signaling pathway. Upregulation of LSD1 reversed the effects of salsolinol on AngII-induced HCFs. Salsolinol inhibited LSD1 via regulation of the STAT3/Notch-1 signaling pathway to improve Ang II-induced myocardial fibrosis <i>in vitro</i>.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"26 5","pages":"527"},"PeriodicalIF":0.0,"publicationDate":"2023-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ae/e7/etm-26-05-12226.PMC10587875.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49695346","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":"Comparison of net adverse clinical events between bivalirudin and heparin as anticoagulants for percutaneous coronary intervention in Chinese patients.","authors":"Lina Chai,&nbsp;Jinjun Liu,&nbsp;Yapei Zhang,&nbsp;Mengying Zhang,&nbsp;Zhenzhen Wang,&nbsp;Yiping Wu,&nbsp;Zhichao Bai,&nbsp;Zhenpeng Qin","doi":"10.3892/etm.2023.12229","DOIUrl":"10.3892/etm.2023.12229","url":null,"abstract":"<p><p>Bivalirudin, as a direct thrombin inhibitor, is considered to be safer compared with other anticoagulants, such as heparin; however, relevant data in China are unclear. The present study aimed to compare the safety of bivalirudin and heparin as anticoagulants in Chinese patients who underwent percutaneous coronary intervention (PCI). In the present study, 2,377 patients with ST-segment elevation myocardial infarction (STEMI), unstable angina, non-STEMI or stable coronary artery disease who underwent primary PCI while receiving bivalirudin or heparin (low molecular weight heparin or unfractionated heparin) were reviewed, and then analyzed as the bivalirudin group (n=944) and heparin group (n=1,433). The net adverse clinical events (NACEs) within 30 days were obtained, which were defined as major adverse cardiac and cerebral events (MACCEs) + Bleeding Academic Research Consortium (BARC) grade 2-5 bleeding events. Compared with the heparin group, the incidence of NACEs was reduced in the bivalirudin group (9.3 vs. 13.4%; P=0.003). However, no discrepancy was found in the incidence of MACCEs between the groups (5.9 vs. 7.6%; P=0.116). Moreover, the incidences of BARC 2-5 (4.8 vs. 8.7%; P<0.001) and BARC 3-5 bleeding events (1.9 vs. 4.4%; P=0.001) were decreased in the bivalirudin group compared with the heparin group. Following adjustment using multivariate logistic regression analysis, bivalirudin treatment (vs. heparin treatment) was independently associated with lower risks of NACEs [odds ratio (OR), 0.587; P<0.001], MACCEs (OR, 0.689; P=0.041) and BARC 2-5 (OR, 0.459; P<0.001) and 3-5 bleeding events (OR, 0.386; P=0.002). Overall, the present study demonstrated that bivalirudin decreased the risks of NACEs and bleeding events compared with heparin in Chinese patients who undergo PCI. However, further validation is required.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"26 5","pages":"530"},"PeriodicalIF":0.0,"publicationDate":"2023-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/85/88/etm-26-05-12229.PMC10587863.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49695416","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":"Association of serum levels of vascular endothelial growth factor and placental growth factor in early threatened abortion and premature delivery: A case‑control study.","authors":"Pei Zhang,&nbsp;Yanqi Jin,&nbsp;Xiaohong Hu","doi":"10.3892/etm.2023.12228","DOIUrl":"10.3892/etm.2023.12228","url":null,"abstract":"<p><p>Vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) serve key roles in the regulation of vascular development, revascularization and vasopermeability in the endometrium, decidua and trophoblasts. Furthermore, both VEGF and PlGF are modulators of embryonic vascular development. Thus, the present study aimed to investigate the serum levels of VEGF and PlGF in female patients with early threatened abortion (TA) who experienced preterm delivery. The present case-control study included 130 pregnant patients with or without TA that were admitted to The Maternal and Childcare Hospital of Nantong University from January 2019 to January 2022. Patients were divided into two groups: i) Group A, which included 55 patients diagnosed with TA with slight vaginal bleeding and closed cervical internal os within the first 6-12 weeks of pregnancy; and ii) group B, which included 75 patients with healthy asymptomatic pregnancy. Blood samples were obtained from all patients and VEGF and PlGF levels were examined prior to treatment, and the chi-squared, Student's t-test and two-way ANOVA followed by Bonferroni's post hoc analysis were used to analyze statistical differences between the two patient groups. Results of the present study demonstrated that patients with TA had significantly lower levels of VEGF and PlGF, compared with the controls. In patients with or without TA, the levels of serum PlGF in the preterm delivery group were significantly decreased compared with patients that did not experience preterm delivery. However, there was no significant difference in the levels of VEGF between patients with or without preterm delivery. In addition, lower levels of PlGF, compared with those in patients without TA, may be associated with an increased risk of preterm delivery in patients without early TA.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"26 5","pages":"529"},"PeriodicalIF":0.0,"publicationDate":"2023-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/fa/18/etm-26-05-12228.PMC10587882.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49695413","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":"Endometrial cell‑derived exosomes facilitate the development of adenomyosis via the IL‑6/JAK2/STAT3 pathway.","authors":"Xinchan Jiang,&nbsp;Xiaobo Chen","doi":"10.3892/etm.2023.12225","DOIUrl":"10.3892/etm.2023.12225","url":null,"abstract":"<p><p>Interleukin (IL)-6 upregulation is involved in the pathogenesis of adenomyosis, but the underlying mechanism remains to be elucidated. Exosomes mediate intercellular communication, therefore the present study investigated whether endometrial cell-derived exosomes mediated the crosstalk between the endometrium and the myometrium via IL-6 signaling. Primary adenomyotic myometrial (AM) cells and eutopic endometrial cells were isolated from patients with adenomyosis. Exosomes were obtained from endometrial cells and incubated with AM cells in the presence or absence of tocilizumab (an IL-6 inhibitor). MTT, flow cytometry and wound-healing assays were performed to examine AM cell proliferation, apoptosis, cell cycle distribution and migration. Western blotting and reverse transcription-quantitative PCR were conducted to determine the expression of the IL-6/Janus kinase 2 (JAK2)/STAT3 pathway proteins. Incubation with endometrial cell exosomes suppressed cell apoptosis of AM cells compared with controls, accompanied by increases in IL-6 production and JAK2/STAT3 phosphorylation. Endometrial cell exosomes promoted cell proliferation, increased the percentage of S-phase cells and enhanced the migration of AM cells. These effects were completely reversed by tocilizumab, along with substantial decreases in IL-6 production and JAK2/STAT3 phosphorylation. Endometrial cell-derived exosomes promote cell proliferation, migration and cell cycle transition of AM cells through IL-6/JAK2/STAT3 activation, facilitating the development of adenomyosis by mediating the crosstalk between the endometrium and the myometrium, and IL-6 targeted therapy could be a complementary approach against adenomyosis.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"26 5","pages":"526"},"PeriodicalIF":0.0,"publicationDate":"2023-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/c6/33/etm-26-05-12225.PMC10587878.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49695418","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":"Myasthenia gravis as initial presentation of a pancreatic neuroendocrine tumor: A case report.","authors":"Elena Stingu, Jerome-Maurice Dobrowolski, Paula Bombach, Dominik Nann, Stephan Singer, Marius Horger, Ulrich M Lauer, Lars Zender, Clemens Hinterleitner, Martina Hinterleitner","doi":"10.3892/etm.2023.12222","DOIUrl":"10.3892/etm.2023.12222","url":null,"abstract":"<p><p>Myasthenia gravis (MG) is a heterogeneous autoimmune disease, which is characterized by a postsynaptic neuromuscular transmission defect, with antibodies directly targeting the acetylcholine receptor (AChR) or other structural proteins of the neuromuscular junction. The majority of MG cases are associated with thymic pathologies, including thymoma, thyroiditis, autoimmune diseases or malignant hematologic neoplasia. The present study reported a rare case of AChR-positive and late-onset ocular MG, which rapidly progressed to a generalized myasthenic syndrome as an initial presentation of a pancreatic neuroendocrine neoplasia (pNEN). Following complete surgical resection of the pNEN, the myasthenic syndrome was improved and the anti-AChR antibody titers were reduced. It has been reported that MG is a paraneoplastic syndrome in thymic neoplasms and less common in hematologic malignancies. However, currently, only few cases of MG as initial presentation of a solid tumor, and more particular of a neuroendocrine neoplasm, have been reported in the literature. In conclusion, surveillance for extrathymic solid malignancies in newly diagnosed patients with MG could promote the early diagnosis of associated tumor diseases.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"26 5","pages":"523"},"PeriodicalIF":0.0,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/83/09/etm-26-05-12222.PMC10580239.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49686582","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":"Rosuvastatin plus ticagrelor decreases the risk of major adverse cardiovascular events and elevates cardiac function compared with ticagrelor alone in patients undergoing percutaneous coronary intervention: A meta‑analysis.","authors":"Jinling Sun,&nbsp;Xiaodong Jin,&nbsp;Limei Zhang,&nbsp;Hongshuai Shen,&nbsp;Hui Yu","doi":"10.3892/etm.2023.12224","DOIUrl":"10.3892/etm.2023.12224","url":null,"abstract":"<p><p>Several previous studies have reported that rosuvastatin plus ticagrelor is superior to ticagrelor monotherapy in patients receiving percutaneous coronary intervention (PCI); several others, however, dispute this. The present meta-analysis summarized relevant studies, aiming to comprehensively explore the efficacy of rosuvastatin plus ticagrelor vs. ticagrelor monotherapy in patients receiving PCI. Published studies comparing the efficacy between rosuvastatin plus ticagrelor and ticagrelor alone among patients receiving PCI were searched in the CNKI, Wanfang, CQVIP, EMBASE, Cochrane and PubMed databases until January 2023. The present meta-analysis included 3 cohort studies and 4 randomized controlled trials with 426 patients receiving rosuvastatin plus ticagrelor and 424 patients receiving ticagrelor monotherapy. Rosuvastatin plus ticagrelor decreased the occurrence of major adverse cardiovascular events (MACE) compared with ticagrelor [relative risk (RR), 0.29; 95% confidence interval (CI), 0.18-0.47]. Subgroup analysis revealed similar findings in studies with a follow-up of <6 months (RR, 0.24; 95% CI, 0.13-0.47) and ≥6 months (RR, 0.36; 95% CI, 0.18-0.70), as well as in studies using 10 mg rosuvastatin (RR, 0.27; 95% CI, 0.15-0.50) and 20 mg rosuvastatin (RR, 0.33; 95% CI, 0.16-0.69). In addition, rosuvastatin plus ticagrelor decreased the left ventricular (LV) end-systolic diameter [mean difference (MD), -0.71; 95% CI, -(1.36-0.07)], LV end-diastolic diameter [MD, -1.17; 95% CI, -(1.91-0.43)] and N-terminal pro-B-type natriuretic peptide [MD, -2.97; 95% CI, -(4.55-1.38)], and increased the LV ejection fraction (MD, 0.99; 95% CI, 0.74-1.25). In conclusion, rosuvastatin plus ticagrelor was shown to decrease the risk of MACE and elevate cardiac function compared with ticagrelor monotherapy in patients receiving PCI.</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"26 5","pages":"525"},"PeriodicalIF":0.0,"publicationDate":"2023-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/21/3f/etm-26-05-12224.PMC10587883.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49695345","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":"[Retracted] Role of microRNA‑210 in human intervertebral disc degeneration.","authors":"Da-Ying Zhang,&nbsp;Zhi-Jian Wang,&nbsp;Yan-Bo Yu,&nbsp;Yong Zhang,&nbsp;Xue-Xue Zhang","doi":"10.3892/etm.2023.12210","DOIUrl":"10.3892/etm.2023.12210","url":null,"abstract":"<p><p>[This retracts the article DOI: 10.3892/etm.2016.3176.].</p>","PeriodicalId":94002,"journal":{"name":"Experimental and therapeutic medicine","volume":"26 5","pages":"511"},"PeriodicalIF":0.0,"publicationDate":"2023-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10570760/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41242585","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}