Molecular medicine reports最新文献

{"title":"Progress on quinoline‑based antitumour agents: Mechanistic insights and optimization strategies (Review).","authors":"Yuwen Zeng, Yutong Yan, Shiye Wu, Wanshan Wu, Ke Chen, Youyi Lai, Qing Ye, Nan Zhang, Yuanyuan Zhou","doi":"10.3892/mmr.2026.14031","DOIUrl":"10.3892/mmr.2026.14031","url":null,"abstract":"<p><p>Quinoline derivatives are a class of heterocycles featuring a fused benzene‑pyridine scaffold that have attracted notable interest in anticancer drug discovery owing to their favourable physicochemical properties, structural versatility and broad biological activities. Accumulating evidence indicates that quinoline‑based compounds exert antitumour effects through several targets and pathways, including via epigenetic regulation, interference with DNA topology, inhibition of signalling pathways, immune modulation, induction of autophagy and targeting of the cytoskeleton. Structure‑activity relationship (SAR) analyses demonstrate that the electronic effects and steric configurations of substituents on the quinoline ring critically determine potency, selectivity and metabolic stability. In particular, oxygenated, halogenated and strongly electron‑withdrawing groups, as well as nitrogen‑containing heterocyclic substituents, enhance hydrophobic interactions or hydrogen bonding with biological targets, thereby improving inhibitory efficacy. Consequently, the quinoline scaffold has emerged as a rated structural motif in anticancer lead compound discovery. Multidimensional optimisation strategies have been proposed to improve the pharmacokinetic profiles and clinical applicability of quinoline derivatives. Nanocarriers and smart stimuli‑responsive delivery systems markedly enhance solubility, circulation time and tumour targeting, whereas prodrug approaches employing enzyme‑sensitive, pH‑responsive or redox‑activated linkers enable selective activation at tumour sites. Combination therapies also exploit the multi‑pathway activity of quinoline derivatives, enhancing antitumour responses and delaying resistance when combined with immunotherapy, chemotherapy or radiotherapy. Furthermore, artificial intelligence and machine learning approaches have shown increasing utility in virtual screening, quantitative structure‑activity relationship modelling and multi‑objective optimisation, accelerating the identification of potent, low toxicity and synthetically accessible candidates. Overall, quinoline derivatives offer systemic advantages as multi‑target anticancer agents. The present review summarises recent advances in molecular mechanisms, SAR insights and drug design strategies, providing a comprehensive framework for advancing quinoline‑based agents towards next‑generation precision anticancer therapies.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13647448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149039794","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":"[Expression of Concern] <i>Ganoderma lucidum</i> polysaccharide inhibits prostate cancer cell migration via the protein arginine methyltransferase 6 signaling pathway.","authors":"Xiaohui Zhao, Dayu Zhou, Yunen Liu, Chun Li, Xiaoguang Zhao, Ying Li, Wei Li","doi":"10.3892/mmr.2026.14010","DOIUrl":"10.3892/mmr.2026.14010","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the histological images shown in Fig. 1B on p. 149, the \"Ctrl\" and \"GLPs 5μg/ml\" data panels contained an overlapping section of data, suggesting that these data panels were derived from the same original source where different experimental conditions were reported. In addition, a concern was raised regarding the antibody that had been used to probe for p21 in the western blot experiments in Fig. 5 (cat. no. sc‑136020, purchased from Santa Cruz Biotechnology, Inc.), since apparently this antibody is specific for a different protein, sometimes referred to as p21‑ARC, which is related to the actin cytoskeleton. The authors have been contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in their paper, and we are awaiting their response. Due to the fact that we have been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Molecular Medicine Reports 17: 147‑157, 2018; DOI: 10.3892/mmr.2017.7904].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13587023/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945403","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":"Artemisinin and its derivatives for metabolic syndrome: From multi‑target mechanisms to translational opportunities (Review).","authors":"Shuo Cao, Mo Yang, Siyu Qu, Jinsong Wu, Jiaheng Li, Ying Zhao","doi":"10.3892/mmr.2026.14026","DOIUrl":"10.3892/mmr.2026.14026","url":null,"abstract":"<p><p>Metabolic syndrome (MetS) is a complex of disorders, characterized by insulin resistance accompanied by abdominal obesity, dyslipidemia, hypertension and impaired glucose metabolism. This group of conditions notably increases the risk of type 2 diabetes mellitus and cardiovascular or cerebrovascular diseases and has become a major global public health challenge. Current treatments for MetS often fail to meet clinical needs owing to the limitations associated with single‑target therapies and notable side effects. Artemisinin‑based drugs are primarily used as antimalarial drugs but have garnered widespread attention for their broad biological activities. Preclinical evidence suggests that artemisinin and its derivatives improve insulin sensitivity, regulate lipid metabolism, alleviate chronic inflammation and reshape the gut microbiota by modulating multiple metabolism‑related signaling pathways, including AMP‑activated protein kinase, PI3K/Akt, NF‑κB and Toll‑like receptor 4, indicating a potential therapeutic avenue for MetS. However, most of these findings are derived from cell‑based and animal studies, while direct clinical evidence in patients with MetS remains limited. In the present review, the therapeutic potential and core molecular mechanisms of artemisinin and its derivatives for MetS are summarized and the challenges and opportunities for their future clinical translation are discussed.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990487","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] RNAi‑mediated A disintegrin and metalloproteinase 9 gene silencing inhibits the tumor growth of non‑small lung cancer <i>in vitro</i> and <i>in vivo</i>.","authors":"Liang Chang, Fangchao Gong, Youbin Cui","doi":"10.3892/mmr.2026.14018","DOIUrl":"10.3892/mmr.2026.14018","url":null,"abstract":"<p><p>Following the publication of the above paper, it was originally drawn to the Editor's attention by a concerned reader that certain of the tumor images of the mice shown in Fig. 5A on p. 1202 were strikingly similar to tumors that appeared subsequently in a pair of other papers in different journals written by different authors at different research institutes. While the possibility of repeating the experiments shown in Fig. 5 and publishing a corrigendum for this paper featuring revised data in Fig. 5 was considered, a different reader has contacted the Editorial Office to notify us that the western blot data featured in Fig. 1 on p. 1200 were strikingly similar to data that had already appeared in an article in the journal <i>BMC Biomedicine</i> that was also written by different authors at different research institutes.Upon investigating this matter, the concerns of the reader were proven to be well‑founded. Owing to the fact that the contentious data in the above article had already been submitted for publication prior to its submission to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should 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 reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 12: 1197‑1204, 2015; DOI: 10.3892/mmr.2015.3477].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990550","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":"Research advances in the microbiota‑gut‑brain axis and Parkinson's disease (Review).","authors":"Yangping Meng, Qian Liu, Hao Zou, Xingyu Zhu, Xinxin Mi, Sitong Li, Yutian Xia, Yucheng Ma, Qianyu Yang, Jiaxin Peng, Junrui Li, Xingliang Liu, Junli Chen","doi":"10.3892/mmr.2026.14016","DOIUrl":"10.3892/mmr.2026.14016","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a common neurodegenerative disease with diverse pathogenic mechanisms. The microbiota‑gut‑brain axis is closely related to the development of PD, in which non‑motor symptoms are considered to be the early manifestation and exacerbation of the disease. Nevertheless, reliable diagnostic criteria or biomarkers for PD have not been fully developed. The gut microbiota as a key transmitter of the gut‑brain axis, can affect disease progression through a variety of pathways, and may be a potential therapeutic target for PD. Therefore, new strategies have been developed with the aim to prevent and control PD by modulating the intestinal microflora, using tools such as antibiotics, probiotics, prebiotics, dietary interventions, fecal microbiota transplantation and vagus nerve stimulation; however, these interventions also face certain issues and challenges. The present article reviewed the latest research on PD through the microbiome‑gut‑brain axis, offering new angles for understanding and treating the condition.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13586700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945422","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":"High‑fat diet exacerbates hepatic and adipose insulin signaling impairment and ovarian lesions in a rat model of letrozole‑induced polycystic ovary syndrome.","authors":"Sunju So, Sujin Kwon, La Yoon Choi, Dae Yong Kim, Mi Hye Kim","doi":"10.3892/mmr.2026.14019","DOIUrl":"10.3892/mmr.2026.14019","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS) is a multifactorial endocrine disorder characterized by ovarian dysfunction and metabolic abnormalities, including insulin resistance. Letrozole (LET)‑based animal models reproduce hyperandrogenic features but often lack the metabolic phenotype of obesity‑associated PCOS. Therefore, in the present study, a high‑fat diet (HFD) was combined with LET and alterations in insulin signaling in metabolic tissues were examined. Female Sprague‑Dawley rats were assigned to control (CON), LET‑induced PCOS (LV) and HFD plus LV (HLV) groups. Body weight, fasting glucose, serum lipids, histology of the liver, visceral adipose tissue (VAT), ovaries and uterus, pancreatic and ovarian immunofluorescence, and hepatic and VAT quantitative PCR for insulin signaling markers were evaluated. Both LV and HLV groups showed increased body weight and fasting glucose, with impaired hepatic and VAT insulin receptor (INSR)/insulin receptor substrate 1 (IRS‑1)/phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling relative to the CON group, with no significant differences between the LV and HLV groups for these parameters. However, HLV further increased hepatic phosphoenolpyruvate carboxykinase and glucose‑6‑phosphatase, and VAT sterol regulatory element‑binding protein 1c and acetyl‑CoA carboxylase, beyond the levels observed in the LV group, and produced more severe hepatic steatosis and adipocyte hypertrophy compared with the LV group. Ovarian cytochrome P450 family 19 subfamily A member 1 and anti‑Müllerian hormone dysregulation was also more pronounced in the HLV group than in the LV group. By contrast, no significant difference was observed between the LV and HLV groups for serum lipid levels, pancreatic β‑cell area or apoptosis, INSR, IRS1, IRS2, AKT, PI3K, glucose transporter 4, carnitine palmitoyltransferase 1A or acyl‑CoA oxidase 1. These findings indicated that HFD selectively exacerbates specific molecular and histopathological features of PCOS beyond those induced by LET alone, partially recapitulating obesity‑related PCOS and providing a practical preclinical platform for studying the metabolic‑reproductive axis and evaluating interventions targeting insulin resistance.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602842/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990505","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":"Demethylase FTO attenuates atherosclerotic plaque via upregulating ABCA1 and ABCG1 expression by targeting ATG5.","authors":"Fengxia Guo, Mei He, Yaonan Li, Kangning Zhu, Bing Hu","doi":"10.3892/mmr.2026.14025","DOIUrl":"10.3892/mmr.2026.14025","url":null,"abstract":"<p><p>N6‑methyladenosine (m6A), the predominant internal modification in eukaryotic mRNAs, has emerged as a significant epigenetic regulator in atherosclerosis; however, its precise mechanistic contributions remain inadequately elucidated. The present study demonstrated that the m6A demethylase fat mass and obesity‑associated (FTO) regulates autophagy, lipid metabolism and plaque vulnerability by targeting autophagy related 5 (ATG5). FTO knockdown resulted in reduced ATG5 expression, thereby suppressing autophagy and downregulating ATP‑binding cassette transporter A1 (ABCA1) and ATP‑binding cassette sub‑family G member 1 (ABCG1). The regulation of ATG5 expression by FTO occurs through direct binding to its transcripts as well as m6A‑mediated mechanisms. Increased m6A modification on ATG5 mRNA following FTO silencing enhanced its recognition by YTH domain‑containing family 1, leading to transcript degradation and diminished protein levels. Consequently, autophagy and cholesterol efflux pathways were inhibited. <i>In vivo</i> experiments revealed that specific FTO knockdown compromised plaque stability and impaired ATG5‑mediated autophagy, in addition to downregulating ABCA1 and ABCG1. These findings highlighted the FTO‑ATG5‑ABCA1/ABCG1 axis as a critical regulator of autophagy and lipid homeostasis in atherosclerosis.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990534","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] CALB1 enhances the interaction between p53 and MDM2, and inhibits the senescence of ovarian cancer cells.","authors":"Long-Qiao Cao, Ya-Nan Wang, Ming Liang, Mei-Zhou Pan","doi":"10.3892/mmr.2026.14027","DOIUrl":"10.3892/mmr.2026.14027","url":null,"abstract":"<p><p>Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the p16 antibody that the authors reported to have used for the western blot experiment shown in Fig. 4B (cat. no. ab51243) is specific for the protein known as P16 ARC (or ARPC5), not the apoptosis‑associated protein p16INK4a, as was intended. Furthermore, upon performing an independent analysis of the data in this paper in the Editorial Office, it came to light that western blot data featured in Fig. 5 were strikingly similar to data that had already been published in a different paper in the journal <i>Oncotarget</i> that featured no authors in common, and western blot data included in Fig. 1B were also very similar to data in another article, which again featured no authors in common ,that was submitted around the same time to the journal <i>OncoTargets and Therapy</i>. Owing to the fact that the contentious data in the above article had already been published prior to its submission to <i>Molecular Medicine Reports</i>, the Editor has decided that this paper should 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 reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 19: 5097‑5104, 2019; DOI: 10.3892/mmr.2019.10212].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149039489","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":"Electroencephalography research in neuropathic pain (Review).","authors":"Lanling Zhou, Nianshun Liao, Hongmei Wang, Jiaxi Zhao, Haijun Jiang, Shihua Dang, Sixun Yu, Haifeng Shu, Xin Chen","doi":"10.3892/mmr.2026.14033","DOIUrl":"10.3892/mmr.2026.14033","url":null,"abstract":"<p><p>Neuropathic pain (NP), arising from lesions or dysfunction of the somatosensory system, remains a major clinical challenge due to its subjective and multidimensional nature. Traditional pain assessments rely on self‑report scales, which lack objectivity and reproducibility. Electroencephalography (EEG), with its high temporal resolution and accessibility, provides a promising avenue for identifying candidate neurophysiological biomarkers of pain. The current narrative review integrates mechanistic insights and electrophysiological evidence to delineate EEG alterations in NP. Resting‑state θ increases and dominant‑frequency slowing are relatively recurrent in chronic NP, whereas α‑, β‑ and γ‑band findings remain heterogeneous. Network analyses further reveal aberrant prefrontal‑limbic and sensorimotor connectivity, as well as altered cross‑frequency coupling, but the direction and topology of these findings remain dependent on the patient population, recording configuration and analytical metric. Advances in computational EEG analysis, graph theory and machine learning are facilitating exploration of objective, individualized pain assessment frameworks. Emerging portable EEG and multimodal approaches may provide opportunities for future clinical translation. Overall, EEG offers a feasible and dynamic method to bridge subjective pain perception with measurable neurophysiological signatures, paving the way toward precision diagnostics and neuromodulation in NP.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 5","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13647446/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112172","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":"Mitochondrial quality control in acute liver injury and its therapeutic implications (Review).","authors":"Ziqiang Chen, Yunhe Wang, Yijing Li, Gang Cong, Yunhang Chu, Yunhui Bai, Yishuo Zhang, Liya Zhou","doi":"10.3892/mmr.2026.13984","DOIUrl":"10.3892/mmr.2026.13984","url":null,"abstract":"<p><p>Acute liver injury (ALI) is a clinically important syndrome with limited mechanism‑based therapies. Notably, mitochondrial dysfunction is increasingly recognized as a central driver of hepatocellular damage and repair failure. The present narrative review aims to summarize the current evidence on mitochondrial quality control (MQC) in ALI, with an emphasis on mitophagy, mitochondrial biogenesis, mitochondrial dynamics, etiology‑specific regulation and therapeutic implications. For the present review, relevant experimental and translational studies addressing MQC‑related mechanisms and interventions in major forms of ALI, including drug‑induced liver injury, ischemia‑reperfusion injury and viral ALI, were reviewed and integrated. The findings indicated that MQC operates as an interconnected network rather than as isolated pathways. Mitophagy, mitochondrial dynamics and mitochondrial biogenesis are temporally coordinated to remove damaged mitochondria, remodel mitochondrial networks and restore bioenergetic capacity. However, MQC responses differ across ALI etiologies, and inappropriate or excessive activation may become maladaptive. In conclusion, understanding MQC as a dynamic and context‑dependent repair system may provide a conceptual basis for precision interventions in ALI. Future studies should clarify spatiotemporal MQC regulation, establish reliable biomarkers and validate MQC‑targeted therapies in clinically relevant settings.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 4","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13469799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685190","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}