Molecular medicine reports最新文献_第9页

Oxymatrine attenuates pulmonary fibrosis via APE1‑mediated regulation of the PINK1/Parkin pathway. 氧化苦参碱通过APE1介导的PINK1/Parkin通路调节减轻肺纤维化。

IF 3.5 3区医学

Molecular medicine reports Pub Date : 2025-10-01 Epub Date: 2025-07-25 DOI: 10.3892/mmr.2025.13627

Wenya Xu, Tian Xie, Bingli Zhang, Jie Zhao, Lei Zhang, Yamei Zheng, Yipeng Ding

{"title":"Oxymatrine attenuates pulmonary fibrosis via APE1‑mediated regulation of the PINK1/Parkin pathway.","authors":"Wenya Xu, Tian Xie, Bingli Zhang, Jie Zhao, Lei Zhang, Yamei Zheng, Yipeng Ding","doi":"10.3892/mmr.2025.13627","DOIUrl":"10.3892/mmr.2025.13627","url":null,"abstract":"Pulmonary fibrosis (PF) is a chronic, progressive lung disease characterized by impaired gas exchange and respiratory difficulties, which can ultimately lead to respiratory failure and mortality. The present study explored the therapeutic effects and underlying mechanisms of oxymatrine (OMT) in an 8‑week‑old C57BL/6 mouse model of bleomycin‑induced PF. The results demonstrated that OMT alleviated lung tissue damage, inflammation and collagen deposition, while promoting autophagy and restoring mitochondrial function. OMT achieved these effects by upregulating apurinic/apyrimidinic endonuclease‑1 (APE1) and activating the PTEN‑induced kinase 1 (PINK1)/Parkin pathway, both of which are key for mitochondrial autophagy. Furthermore, Lewis lung carcinoma mouse lung cancer cells were transduced with an adeno-associated virus containing small interfering RNA APE1 and a negative control, and the silencing efficiency was validated by reverse transcription‑quantitative PCR and western blotting. The results revealed a significant reduction in APE1 expression in the APE1 knockdown group compared with that in the negative control knockdown group. Immunohistochemistry and immunofluorescence confirmed that OMT increased the expression of APE1, PINK1 and Parkin while reducing markers of fibrosis, such as α‑smooth muscle actin and collagen type I α 1. However, silencing APE1 or inhibiting mitochondrial autophagy with mitochondrial division inhibitor‑1 reversed the beneficial effects of OMT, suggesting a key role for APE1 and the PINK1/Parkin pathway in its mechanism of action. These findings provide insights into the antifibrotic potential of OMT and highlight its potential as a basis for the development of new therapies for PF.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12311560/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144708205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Research advances in current drugs targeting hyperlipidemia (Review). 高脂血症药物研究进展（综述）。

IF 3.5 3区医学

Molecular medicine reports Pub Date : 2025-10-01 Epub Date: 2025-07-19 DOI: 10.3892/mmr.2025.13623

Hanwei Zhao, Yao Wang, Yaqing Li, Ran Cheng, Wenge Chen

{"title":"Research advances in current drugs targeting hyperlipidemia (Review).","authors":"Hanwei Zhao, Yao Wang, Yaqing Li, Ran Cheng, Wenge Chen","doi":"10.3892/mmr.2025.13623","DOIUrl":"10.3892/mmr.2025.13623","url":null,"abstract":"Hyperlipidemia is a disorder of lipid metabolism. With rapid economic development, unhealthy diets and lack of exercise, the incidence of hyperlipidemia has been increasing year by year. In adults, hyperlipidemia is a major risk factor for cardiovascular diseases, especially atherosclerotic cardiovascular disease (ASCVD), and the current goal of treating hyperlipidemia is to prevent and manage ASCVD. In terms of etiology, hyperlipidemia is divided into primary and secondary types. Common primary hyperlipidemias include familial hypercholesterolemia, mixed familial hyperlipidemia, type III hyperlipoproteinemia and familial chylomicronemia syndrome. In addition to statins, ezetimibe and proprotein convertase subtilisin/kexin type 9 inhibitors, a number of new and emerging drugs for lowering cholesterol and triglycerides are being developed to regulate lipid levels and prevent cardiovascular diseases. The present review summarized the classification and composition of lipoproteins, the pathogenesis of common primary hyperlipidemias, secondary factors affecting dyslipidemia, modern common lipid‑lowering drugs and the latest clinical progress in emerging lipid‑lowering therapies.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 4","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12308852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668024","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

AZD1080, a specific inhibitor of GSK‑3β, inhibits stemness and malignancies in osteosarcoma cancer stem‑like cells. AZD1080是GSK - 3β的特异性抑制剂，可抑制骨肉瘤癌症干细胞样细胞的干性和恶性肿瘤。

IF 3.5 3区医学

Molecular medicine reports Pub Date : 2025-09-01 Epub Date: 2025-07-11 DOI: 10.3892/mmr.2025.13613

Peiyu Guo, Zhenkai Lou, Hongda Gong, Xiaodong Hou, Chunqiang Zhang, Bing Wang, Kaili Du

{"title":"AZD1080, a specific inhibitor of GSK‑3β, inhibits stemness and malignancies in osteosarcoma cancer stem‑like cells.","authors":"Peiyu Guo, Zhenkai Lou, Hongda Gong, Xiaodong Hou, Chunqiang Zhang, Bing Wang, Kaili Du","doi":"10.3892/mmr.2025.13613","DOIUrl":"10.3892/mmr.2025.13613","url":null,"abstract":"Osteosarcoma is the most common primary bone cancer, primarily affecting children and young adults. Cancer stem cells (CSCs), a subpopulation presenting stemness, critically influence prognosis and promote recurrence and metastasis. Due to the crucial role of glycogen synthase kinase‑3 beta (GSK‑3β) in maintaining stemness, it is considered as an important target for drug development. The aim of the present study was to evaluate the inhibitory effect of AZD1080, a GSK‑3β inhibitor, on osteosarcoma CSCs. AZD1080 treatment clearly inhibited sphere formation in U2OS and 143B cells and dissociated spheres in CSCs derived from U2OS and 143B; in both processes, stemness markers OCT4 and SOX2 were markedly decreased, without affecting cell proliferation or apoptosis. AZD1080 treatment inhibited phosphorylation of GSK‑3β and its downstream regulated genes, including HEY1, HES1, CyclinD1 and β‑catenin. It was also observed that GSK‑3β activity was critical for the inhibitory effects of AZD1080 treatment on sphere formation and stemness. Moreover, GSK‑3β knockdown inhibited sphere formation and invasion capacity, indicating that AZD1080 exerts inhibitory roles in a GSK‑3β‑dependent manner. Taken together, the results showed AZD1080 as a specific inhibitor of CSC stemness, without cytotoxicity, and indicated it was a promising therapeutic agent that targeted GSK‑3β signaling in osteosarcoma.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 3","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12272150/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Blocking the IL‑6 pathway to treat immune checkpoint inhibitor‑induced inflammatory arthritis (Review). 阻断IL - 6通路治疗免疫检查点抑制剂诱导的炎性关节炎（综述）

IF 3.5 3区医学

Molecular medicine reports Pub Date : 2025-09-01 Epub Date: 2025-07-11 DOI: 10.3892/mmr.2025.13615

Liwen Zhao, Chuting Feng, Yong-Jing Gao, Tianzhen He

引用次数: 0

[Retracted] PADI4‑mediated epithelial‑mesenchymal transition in lung cancer cells. 肺癌细胞中PADI4介导的上皮-间充质转化

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-09-01 Epub Date: 2025-07-11 DOI: 10.3892/mmr.2025.13610

Meiyan Liu, Yang Qu, Xue Teng, Ying Xing, Dandan Li, Chunhong Li, Li Cai

{"title":"[Retracted] PADI4‑mediated epithelial‑mesenchymal transition in lung cancer cells.","authors":"Meiyan Liu, Yang Qu, Xue Teng, Ying Xing, Dandan Li, Chunhong Li, Li Cai","doi":"10.3892/mmr.2025.13610","DOIUrl":"10.3892/mmr.2025.13610","url":null,"abstract":"Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the western blot data shown in Fig. 5C on p. 5092 were strikingly similar to data that had already been published in different form in the journal Oncotarget in an article written by different authors. In addition, upon analyzing the data in this paper independently in the Editorial Office, one pair of overlapping data panels was identified comparing the scratch‑wound assay data in Fig. 2A with that in Fig. 4A, whereas two pairs of overlapping data panels were identified for the invasion assay data shown in Fig. 4B (thereby affecting all the panels), such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original source. Owing to the fact that the contentious western blot data mentioned above in Fig. 5C had already apparently been published prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. After contacting the authors, they accepted the decision to retract the paper. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 19: 3087‑3094, 2019; DOI: 10.3892/mmr.2019.9968].","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12272154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Retracted] Placenta‑derived mesenchymal stem cells improve airway hyperresponsiveness and inflammation in asthmatic rats by modulating the Th17/Treg balance. 胎盘源性间充质干细胞通过调节Th17/Treg平衡改善哮喘大鼠气道高反应性和炎症。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-09-01 Epub Date: 2025-06-27 DOI: 10.3892/mmr.2025.13601

Yingying Li, Hongbo Li, Yinyin Cao, Fuling Wu, Wenbin Ma, Yuesi Wang, Shuzhen Sun

{"title":"[Retracted] Placenta‑derived mesenchymal stem cells improve airway hyperresponsiveness and inflammation in asthmatic rats by modulating the Th17/Treg balance.","authors":"Yingying Li, Hongbo Li, Yinyin Cao, Fuling Wu, Wenbin Ma, Yuesi Wang, Shuzhen Sun","doi":"10.3892/mmr.2025.13601","DOIUrl":"10.3892/mmr.2025.13601","url":null,"abstract":"Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the flow cytometric plots shown in Fig. 4A and B, and Fig. 4D and E, respectively on p. 8142, these two pairs of plots appeared to show similar groupings of dots, which would not have been anticipated if these experiments had been performed discretely under different experimental conditions, suggesting a fundamental flaw either in the way in which these experiments were performed or in how the results were outputted. The Editor of Molecular Medicine Reports has decided that this paper should be retracted from the Journal on account of a lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 16: 8137‑8145, 2017; DOI: 10.3892/mmr.2017.7605].","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12218044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144506846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

SLC7A1, SGK1 and HMGB2 are overexpressed in cervical cancer tissues and the miR‑23b‑3p/HMGB2 axis regulates cell migration and invasion. SLC7A1、SGK1和HMGB2在宫颈癌组织中过表达，miR‑23b‑3p/HMGB2轴调控细胞迁移和侵袭。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-09-01 Epub Date: 2025-06-27 DOI: 10.3892/mmr.2025.13600

Gladys Wendy Valente-Niño, Hilda Jiménez-Wences, Manuel Joaquín Romero-López, Judit Alarcón-Millán, Miguel Ángel Mendoza-Catalán, Oscar Peralta-Zaragoza, Daniel Hernández-Sotelo, Carlos Pérez-Plasencia, Gloria Fernández-Tilapa

{"title":"SLC7A1, SGK1 and HMGB2 are overexpressed in cervical cancer tissues and the miR‑23b‑3p/HMGB2 axis regulates cell migration and invasion.","authors":"Gladys Wendy Valente-Niño, Hilda Jiménez-Wences, Manuel Joaquín Romero-López, Judit Alarcón-Millán, Miguel Ángel Mendoza-Catalán, Oscar Peralta-Zaragoza, Daniel Hernández-Sotelo, Carlos Pérez-Plasencia, Gloria Fernández-Tilapa","doi":"10.3892/mmr.2025.13600","DOIUrl":"10.3892/mmr.2025.13600","url":null,"abstract":"MicroRNA (miRNA/miR)‑124‑3p and miR‑23b‑3p are tumor suppressor miRNAs that are associated with advanced cervical cancer (CC), regulating proliferation, migration, invasion, apoptosis and metastasis; however, the identity and function of the various genes regulated by these miRNAs remain unknown. The present study predicted the specific and shared targets of miR‑124‑3p and miR‑23b‑3p, cellular processes and signaling pathways involving the predicted targets. SLC7A1 was found among the shared targets, SGK1 among the targets of miR‑124‑3p and HMGB2 as a target of miR‑23b‑3p. SLC7A1, SGK1 and HMGB2 mRNA expression was markedly increased in patients with cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC) and levels of SGK1 and HMGB2 were associated with CC progression. SLC7A1, SGK1 and HMGB2 interact with proteins involved in cellular processes associated with cancer progression. Overexpression of miR‑124‑3p decreased mRNA of SLC7A1 in C‑33A cells, and of SGK1 in both cell lines. Ectopic expression of miR‑23b‑3p decreased HMGB2 levels in C‑33A and CaSki, and reduced cell migration and invasion. HMGB2 knockdown experiments revealed that HMGB2 modulates migration and invasion of CC cell lines. In conclusion, the results of the present study suggest that miR‑124‑3p and miR‑23b‑3p modulate processes associated with carcinogenesis and tumor progression through their individual and shared target mRNAs and that the miR‑23b‑3p/HMGB2 axis is among the mechanisms that modulate migration and invasion in CC.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12218049/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144506847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

circRNA hsa_circ_0072107 aggravates myocardial hypertrophy via its function as a competitive endogenous RNA of miR‑516b‑5p. circRNA hsa_circ_0072107通过其作为miR - 516b - 5p竞争内源性RNA的功能加重心肌肥大。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-09-01 Epub Date: 2025-06-20 DOI: 10.3892/mmr.2025.13597

Rui Wang, Yongli He, Wuxia Ma, Jindong Xu, Qi Zhong, Cheng Huang

{"title":"circRNA hsa_circ_0072107 aggravates myocardial hypertrophy via its function as a competitive endogenous RNA of miR‑516b‑5p.","authors":"Rui Wang, Yongli He, Wuxia Ma, Jindong Xu, Qi Zhong, Cheng Huang","doi":"10.3892/mmr.2025.13597","DOIUrl":"10.3892/mmr.2025.13597","url":null,"abstract":"The present study aimed to identify differentially expressed circRNAs in hypertrophic cardiac tissues and explored the potential regulatory role and mechanism of one differentially expressed circRNA in myocardial hypertrophy. RNA sequencing was used to identify differentially expressed circRNAs in hypertrophic and control cardiac tissues. CircRNA expression levels were verified by reverse transcription‑quantitative PCR. Isoproterenol (ISO) was used to induce hypertrophy of AC16 cells. The extent of cell hypertrophy was indicated by the cell size, protein/DNA ratio and levels of B‑type natriuretic peptide (BNP) and β‑myosin heavy chain (β‑MHC). The interactions between hsa_circ_0072107 and miR‑516b‑5p, as well as between miR‑516b‑5p and zinc ring finger protein 36 (ZFP36), were confirmed through dual luciferase assays, biotinylated probe pull‑down and anti‑AGO2 RNA immunoprecipitation assays. hsa_circ_0072107 was one of the most upregulated circRNAs in hypertrophic cardiac tissues. hsa_circ_0072107 overexpression and ISO treatment increased cell size, elevated the protein/DNA ratio and increased the levels of BNP and β‑MHC in AC16 cells, indicating that hsa_circ_0072107 aggravates AC16 hypertrophy. These changes induced by ISO treatment could be blocked by the knockdown of hsa_circ_0072107. The dual‑luciferase activity assay indicated that miR‑516b‑5p can bind to hsa_circ_0072107. miR‑516b‑5p binding site mutation blocked the effect of hsa_circ_0072107. ZFP36 is a target gene of miR‑516b‑5p, which suppresses AC16 hypertrophy. hsa_circ_0072107 overexpression alleviated the effect of miR‑516b‑5p overexpression on cell hypertrophy and ZFP36 expression. hsa_circ_0072107 is up‑regulated in hypertrophic cardiac tissues and potentially promotes AC16 hypertrophy and may play its role by acting as a competitive endogenous RNA of miR‑516b‑5p. Thus, hsa_circ_0072107 may be a novel target for the treatment of myocardial hypertrophy.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12203038/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Polygonatum sibiricum polysaccharide alleviates liver fibrosis through the TGF‑β/Smad signaling pathway and reduces collagen. 黄精多糖通过TGF - β/Smad信号通路减轻肝纤维化，减少胶原。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-09-01 Epub Date: 2025-06-20 DOI: 10.3892/mmr.2025.13599

Yin Yuan, Xiaojing Liu, Tian Zhou, Zhongguang Zhou, Minghai Gong, Yihang Li

{"title":"Polygonatum sibiricum polysaccharide alleviates liver fibrosis through the TGF‑β/Smad signaling pathway and reduces collagen.","authors":"Yin Yuan, Xiaojing Liu, Tian Zhou, Zhongguang Zhou, Minghai Gong, Yihang Li","doi":"10.3892/mmr.2025.13599","DOIUrl":"10.3892/mmr.2025.13599","url":null,"abstract":"Liver fibrosis (LF) is a liver condition that represents a serious health risk to humans, and effective therapeutic options are limited. Polygonatum sibiricum polysaccharide (PSP), derived from the roots of P. sibiricum Red, has been demonstrated to exert anti‑inflammatory, antioxidant and antibacterial effects. However, its potential therapeutic impact on LF remains unexplored. In the present study, LF model rats were established through subcutaneous injection of carbon tetrachloride combined with a high‑fat diet and alcohol administration. Following the induction of fibrosis, rats in the PSP and Biejia ruangan (BJRG) treatment groups received daily intragastric doses of PSP and BJRG, respectively, for a duration of 4 weeks. The control and model groups were administered an equivalent volume of water. Liver function was evaluated through biochemical analyses, whereas hepatopathological alterations were assessed using hematoxylin and eosin and Masson's trichrome staining. Levels of inflammatory and oxidative stress markers were quantified using ELISA. Hepatic collagen synthesis and degradation were examined using ELISA and immunohistochemistry. Furthermore, the expression of genes and proteins associated with the TGF‑β/Smad signaling pathway were analyzed by reverse transcription‑quantitative PCR and western blotting. The results indicated that PSP exerts anti‑fibrotic effects, primarily through anti‑inflammatory and antioxidant mechanisms. Moreover, PSP appeared to promote the degradation and inhibit the synthesis of hepatic collagen fibers, potentially through modulation of the TGF‑β/Smad signaling pathway.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"32 3","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12215250/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Retracted] Isorhamnetin inhibits IL‑1β‑induced expression of inflammatory mediators in human chondrocytes. [撤回]异鼠李素抑制IL - 1β诱导的人软骨细胞炎症介质的表达。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-09-01 Epub Date: 2025-06-20 DOI: 10.3892/mmr.2025.13595

Jin Li, Ruishan Wu, Xiaoping Qin, Dongyang Liu, Fenjie Lin, Qinglu Feng

引用次数: 0