Molecular medicine reports最新文献

{"title":"Curcumin ameliorates cerulein‑induced chronic pancreatitis through Nrf‑2/HO‑1 signaling.","authors":"Dong-Uk Kim, Bitna Kweon, Jin-Young Oh, Gyeong-Ran Noh, Yebin Lim, Jihyun Yu, Myoung-Jin Kim, Dong-Gu Kim, Sung-Joo Park, Gi-Sang Bae","doi":"10.3892/mmr.2025.13501","DOIUrl":"10.3892/mmr.2025.13501","url":null,"abstract":"<p><p>Chronic pancreatitis (CP) is an invasive inflammatory disorder characterized by endocrine and exocrine dysfunction. There are currently no effective drugs for the treatment of CP. The present study investigated whether curcumin improves cerulein‑induced CP fibrosis in a mouse model and pancreatic stellate cells (PSCs). The CP mouse model was established by intraperitoneally injecting cerulein (50 µg/kg) for 3 weeks (six times at 1 h intervals/day; 4 days/week). To investigate the effects of curcumin, dimethyl sulfoxide or curcumin was injected intraperitoneally 1 h before the first daily injection of cerulein. To determine the severity of CP, the pancreas was harvested 24 h after the last cerulein injection for histological examination and assessment of PSC activation and collagen deposition. Additionally, levels of the nuclear factor erythroid 2‑related factor 2 (Nrf2) and heme oxygenase‑1 (HO‑1) were evaluated to determine the mechanism underlying the anti‑fibrotic effect of curcumin in PSCs. Curcumin improved pancreatic injury associated with CP by inhibiting PSC activation and collagen deposition. Moreover, curcumin increased HO‑1 expression levels via the activation of Nrf2 in PSCs, which suppressed the activation of PSCs. In conclusion, the present results suggest that curcumin can ameliorate pancreatic fibrosis induced by repetitive cerulein challenges via the induction of HO‑1 and is a beneficial agent for the treatment of CP.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11963747/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143720656","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}

{"title":"[Corrigendum] Effects of nicorandil on p120 expression in the spinal cord and dorsal root ganglion of rats with chronic postsurgical pain.","authors":"Sai-Sai Huang, Su Cao, Cui E Lu, Yi-Bin Qin, Jian-Ping Yang","doi":"10.3892/mmr.2025.13497","DOIUrl":"10.3892/mmr.2025.13497","url":null,"abstract":"<p><p>Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that certain of the figures associated with four separate papers published by the same research group, and featuring some of the same authors, appeared to share immunofluorescence and graphical data. Upon analyzing the data independently in the Editorial Office, as far as the paper above was concerned, the diagram depicting the establishment of the skin/muscle incision and retraction (SMIR) model in rats, as featured in Fig. 1A on p. 4823, also appeared in one of the associated articles in the journal <i>Pain Research and Management</i> a couple of years afterwards. Given that the sharing of the image in question has come to light, the authors wish to present an alternative version of Fig. 1, showing the original photograph depicting the SMIR model in Fig. 1A. This figure is shown below. All the authors agree with the publication of this corrigendum and are grateful to the Editor of <i>Molecular Medicine Reports</i> for allowing them the opportunity to publish this. [Molecular Medicine Reports 22: 4821‑4827, 2020; DOI: 10.3892/mmr.2020.11546].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11948979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143670508","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}

{"title":"Apelin/APJ alleviates diabetic nephropathy by improving glomerular endothelial cells dysfunction via SIRT3‑KLF15.","authors":"Mingcong Huang, Jing Chang, Yu Liu, Jiming Yin, Xiangjun Zeng","doi":"10.3892/mmr.2025.13487","DOIUrl":"10.3892/mmr.2025.13487","url":null,"abstract":"<p><p>Glomerular basement membrane (GBM) thickening, the earliest morphological change of diabetic nephropathy (DN), is related to glomerular endothelial cells (GECs) dysfunction which increase extracellular matrix (ECM) synthesizing. Apelin, the endogenous ligand for apelin/apelin receptor (APJ), is reported to alleviate endothelial cell dysfunction in DN. Therefore, it was hypothesized that apelin/APJ reduced GBM thickening by decreasing the synthesis of ECM in GECs. The results showed that apelin reduced glomerular fibrosis and GBM thickening by decreasing the expression of laminin and collagen IV in diabetic mice, which were cancelled following APJ knockout in GECs. Furthermore, apelin/APJ inhibited the synthesis of laminin and collagen IV in GECs by increasing the expression and activity of SIRT3, which promoted KLF15 deacetylation and translocation into nucleus. In conclusion, apelin/APJ reduced GBM thickening in diabetes mellitus by preventing laminin and collagen IV synthesizing via SIRT3‑KLF15 pathway in GECs.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920778/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573440","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}

{"title":"Redox signaling‑mediated muscle atrophy in ACL injury: Role of physical exercise (Review).","authors":"Yucong Wang, Chunxiao Gu, Hui Zhao, Zhongzheng Li, Anand Thirupathi","doi":"10.3892/mmr.2025.13484","DOIUrl":"10.3892/mmr.2025.13484","url":null,"abstract":"<p><p>Muscle atrophy frequently occurs in patients with anterior cruciate ligament (ACL) injury, despite active participation in muscle strengthening programs. Without appropriate countermeasures such as exercise and pharmacological interventions, the atrophy may worsen. At the cellular and molecular levels, various protein synthesis‑related pathways and redox‑dependent molecules regulate processes associated with atrophy by activating or deactivating key signaling pathways. Muscle atrophy and the associated dysfunction can be reversed by physical exercise, which increases protein synthesis, thereby improving muscle strength and function around the ACL. However, the influence of different features of exercise protocols, including exercise type, intensity and duration, as well as the individual capacity of the patient, on the activity of the aforementioned pathways requires further investigation. Additionally, the mechanism by which redox‑sensitive molecules attenuate atrophy in ACL injury remains to be fully understood. The present review discusses exercise, signaling pathways and muscle atrophy in ACL injury, and highlights potential therapeutic strategies. These findings may also have implications for other joint diseases associated with ACL‑related injury.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11904765/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573448","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}

{"title":"Mitochondria‑derived peptides: Promising microproteins in cardiovascular diseases (Review).","authors":"Yutong Ran, Zhiliang Guo, Lijuan Zhang, Hong Li, Xiaoyun Zhang, Xiumei Guan, Xiaodong Cui, Hao Chen, Min Cheng","doi":"10.3892/mmr.2025.13492","DOIUrl":"10.3892/mmr.2025.13492","url":null,"abstract":"<p><p>Mitochondria‑derived peptides (MDPs) are a unique class of peptides encoded by short open reading frames in mitochondrial DNA, including the mitochondrial open reading frame of the 12S ribosomal RNA type‑c (MOTS‑c). Recent studies suggest that MDPs offer therapeutic benefits in various diseases, including neurodegenerative disorders and types of cancer, due to their ability to increase cellular resilience. Mitochondrial dysfunction is a key factor in the onset and progression of cardiovascular diseases (CVDs), such as atherosclerosis and heart failure, as it disrupts energy metabolism, increases oxidative stress and promotes inflammation. MDPs such as humanin and MOTS‑c have emerged as important regulators of mitochondrial health, as they show protective effects against these processes. Recent studies have shown that MDPs can restore mitochondrial function, reduce oxidative damage and alleviate inflammation, thus counteracting the pathological mechanisms that drive CVDs. Therefore, MDPs hold promise as therapeutic agents that are capable of slowing, stopping, or even reversing CVD progression and their use presents a promising strategy for future treatments. However, the clinical application of MDPs remains challenging due to their low bioavailability, poor stability and high synthesis costs. Thus, it is necessary to improve drug delivery systems to enhance the bioavailability of MDPs. Moreover, integrating basic research with clinical trials is essential to bridge the gap between experimental findings and clinical applications.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625366","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}

{"title":"[Retracted] miR‑23a suppresses pancreatic cancer cell progression by inhibiting PLK‑1 expression.","authors":"Bin Chen, Akao Zhu, Lei Tian, Ying Xin, Xinchun Liu, Yunpeng Peng, Jingjing Zhang, Yi Miao, Jishu Wei","doi":"10.3892/mmr.2025.13475","DOIUrl":"10.3892/mmr.2025.13475","url":null,"abstract":"<p><p>Following the publication of this paper, and subsequently to the publication of a corrigendum (DOI: 10.3892/mmr.2022.12738) that was intended to address the issue of a pair of duplicated data panels in Fig. 2C, it was drawn to the Editor's attention by a concerned reader that there regrettably remained issues with overlapping data panels in the revised version of Fig. 2 that was provided by the authors; furthermore, the revised data that were included in the corrected version of this figure were found to have appeared previously in a paper published in the journal <i>OncoTargets and Therapy</i> featuring different authors at different research institutes, which has subsequently been retracted. In view of the fact that the abovementioned data had already apparently been published prior to its submission to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should now be retracted from the Journal. 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 18: 105-122, 2018; DOI: 10.3892/mmr.2018.8941].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11884215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143523953","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}

{"title":"Dysregulation of the SREBP pathway is associated with poor prognosis and serves as a potential biomarker for the diagnosis of hepatocellular carcinoma.","authors":"Xiaodan Li, Yuhan Wang, Junchi Liu, Tianmiao Gao, Lizhi Cao, Meng Yan, Na Li","doi":"10.3892/mmr.2025.13477","DOIUrl":"10.3892/mmr.2025.13477","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is a severe disease associated with a poor prognosis. The role of aberrant lipid metabolism in the development and progression of HCC necessitates detailed characterization. Sterol regulatory element‑binding proteins (SREBPs), pivotal transcription factors governing lipogenesis, are central to this process. The present study aimed to assess the regulation of HCC by the SREBP signaling pathway, examining the expression levels of genes in this pathway, the clinical implications and its prognostic value using the Kaplan‑Meier method. Pearson's correlation coefficient was used to identify the co‑expression of SREBP pathway genes in HCC. Genomic analysis examined the frequency of TP53 mutations in groups with and without SREBP pathway alterations. In addition, small interfering RNAs targeting genes of the SREBP pathway were transfected into Huh‑7 and HCC‑LM3 cell lines. Subsequently, Cell Counting Kit‑8 and Transwell assays were carried out to evaluate the viability and invasion of these cells. Reverse transcription‑quantitative PCR and western blotting were performed to investigate the expression of TP53 in response to silencing of SREBP pathway genes. Dysregulation of SREBP pathway genes was detected in HCC tissues compared with in normal liver tissues, and predicted a poor prognosis. Silencing these genes reduced the viability and invasion of HCC cells. Furthermore, abnormal SREBP pathway gene expression was associated with poor survival rates, vascular invasion, advanced tumor stage and an increased incidence of TP53 mutations. By contrast, knockdown of SREBP pathway genes decreased mutant TP53 expression at both the mRNA and protein levels in HCC cells. The findings of the present study suggested that SREBP pathway genes could serve as promising prognostic biomarkers for HCC. The combined analysis of individual gene expression levels offers offer novel insights into the pathogenesis and progression of HCC.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894594/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143523901","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}

{"title":"Glycoprotein 130 improves repressor element‑1 silencing transcription factor‑related axon regenerative capacity in peripheral nerves with aging.","authors":"So Kawakita, Kiyohito Naito, Daisuke Kubota, Yuji Ueno, Takako Negishi-Koga, Yasuhiro Yamamoto, Takamaru Suzuki, Norizumi Imazu, Kenjiro Kawamura, Nobutaka Hattori, Muneaki Ishijima","doi":"10.3892/mmr.2025.13486","DOIUrl":"10.3892/mmr.2025.13486","url":null,"abstract":"<p><p>Axon regenerative capacity diminishes with aging and differences in the condition of peripheral nerves between young and elderly individuals have been reported. However, the underlying pathology remains unclear. The expression of repressor element‑1 silencing transcription factor (REST) increases with age and is reported to suppress axon regeneration. The present study investigated the pathology and potential treatment of reduced axon regenerative capacity using REST‑regulated cells and a mouse model. This study examined the molecular expression of the janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3) pathway, which is involved in growth‑associated protein 43 (GAP43) expression. In REST‑overexpressed (REST‑OE), glycoprotein 130 (GP130), JAK1 and phosphorylated STAT3 (p‑STAT3) expression was decreased compared with the control (GP130, P=0.004; JAK1, P=0.038; pSTAT3, P=0.015). On the other hand, in REST‑low expressed (siREST), GP130, JAK1 and pSTAT3 expression was increased compared with the control (GP130, P=0.004; JAK1, P=0.003; pSTAT3, P=0.033). It suggested that GP130 plays an important role. Therefore, GP130 agonist was administered to REST‑OE and aged mice and resulted in a significant increase in GAP43 expression (REST‑OE: Protein P=0.018, mRNA P=0.040; aged mice: Protein P=0.016, mRNA P=0.013). The results of this study suggest that the pathology of reduction in peripheral nerve axon regenerative capacity is inhibited by age‑related increase in REST expression, which leads to decreased GP130 expression and inhibition of JAK1/STAT3 pathway activity. These findings suggest that regulating GP130 expression may improve axon regenerative capacity by aging.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143573441","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}

{"title":"Exosomes derived from baicalin‑pretreated mesenchymal stem cells mitigate atherosclerosis by regulating the SIRT1/NF‑κB signaling pathway.","authors":"Xiaochun Yang, Wei Wu, Weitian Huang, Junfeng Fang, Yunli Chen, Xiaoyan Chen, Xiaolan Lin, Yanbin He","doi":"10.3892/mmr.2025.13491","DOIUrl":"10.3892/mmr.2025.13491","url":null,"abstract":"<p><p>Atherosclerosis (AS) is a disease with high global incidence and mortality rates. Currently, the treatment of AS in clinical practice carries a high risk of adverse effects and toxic side effects. The pretreatment of mesenchymal stem cells (MSCs) with drugs may enhance the bioactivity of MSC‑derived exosomes (MSC‑exos), which could be a promising candidate for inhibiting the progression of AS. The aim of the present study was to investigate the ability of exos derived from baicalin‑preconditioned MSCs (Ba‑exos) to exhibit an inhibitory effect on AS progression and to explore the potential molecular mechanisms. Exos were isolated from untreated MSCs and MSCs pretreated with Ba, and were characterized using transmission electron microscopy, nanoparticle tracking analysis and western blotting. Subsequently, Cell Counting Kit‑8 and Transwell assays, reverse transcription‑quantitative PCR, immunofluorescence, western blotting and ELISA were used to evaluate the effects of Ba‑exos on AS, and the possible molecular mechanisms. Oil Red O and Masson staining were used to assess AS pathological tissue in a high‑fat diet‑induced mouse model of AS. Notably, MSC‑exos and Ba‑exos were successfully isolated. Compared with MSC‑exos, Ba‑exos demonstrated superior inhibitory effects on the viability and migration, and the levels of inflammatory factors in oxidized low‑density lipoprotein (ox‑LDL)‑induced vascular smooth muscle cells (VSMCs). Additionally, compared with MSC‑exos, Ba‑exos significantly inhibited NF‑κB activation by upregulating sirtuin 1 (SIRT1), thereby suppressing inflammation in ox‑LDL‑induced VSMCs to a greater extent. In mice with high‑fat diet‑induced AS, Ba‑exos exhibited the ability to inhibit AS plaque formation and to alleviate AS progression by reducing the levels of inflammatory factors compared with MSC‑exos; however, the difference was not significant. In conclusion, Ba‑exos may serve as a potential strategy for treating AS by regulating the SIRT1/NF‑κB signaling pathway to suppress inflammation.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11924171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625370","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}

{"title":"Fibrosis factor CTGF facilitates VCAM‑1‑dependent monocyte adhesion to osteoarthritis synovial fibroblasts via the FAK and JNK pathways.","authors":"Shan-Chi Liu, Yat-Yin Law, Yu-Ying Wu, Yuan-Li Huang, Chun-Hao Tsai, Wei-Cheng Chen, Chih-Hsin Tang","doi":"10.3892/mmr.2025.13489","DOIUrl":"10.3892/mmr.2025.13489","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a long‑term, degenerative joint disease that presents significant clinical challenges and imposes considerable financial burdens. Fibrosis is closely intertwined with the pathogenesis of various degenerative diseases, including OA. Using data from the GDS5401 dataset, the present study determined that expression levels of the fibrosis factor connective tissue growth factor (CTGF) were significantly higher in OA patients than in normal individuals. The present study also identified CTGF elevated expression levels in both OA patients compared with healthy controls and in rats with anterior cruciate ligament transection‑induced OA versus controls. Stimulating OA synovial fibroblasts (OASFs) with CTGF was shown to promote vascular cell adhesion molecule‑1 (VCAM‑1) production, thereby facilitating monocyte adhesion to OASFs. Analysis of a large dataset revealed that monocytes are the only mononuclear cells with significantly elevated levels in OA patients. It also appeared that CTGF‑induced VCAM‑1 production and monocyte adhesion were mediated via the focal adhesion kinase and JNK pathways. These findings suggest that CTGF contributes to OA progression by enhancing monocyte adhesion to the synovial membrane.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 5","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11920775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143625377","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}