Molecular medicine reports最新文献

{"title":"Erbin deficiency exacerbates sepsis‑induced liver injury through mitochondrial ROS/NLRP3‑mediated inflammatory responses.","authors":"Jing Zuo, Xing Wang, Guoqing Jing, Xiaojing Wu, Xuemin Song","doi":"10.3892/mmr.2026.14045","DOIUrl":"https://doi.org/10.3892/mmr.2026.14045","url":null,"abstract":"<p><p>Sepsis‑induced liver injury (SLI) is a life‑threatening complication of sepsis characterized by microcirculatory dysfunction, oxidative stress, excessive inflammation, and immune dysregulation. However, the role of ErbB2 interacting protein (Erbin) in SLI remains unclear. In the present study, the functional role and underlying mechanism of Erbin were investigated in a cecal ligation and puncture (CLP)‑induced mouse model of SLI using wild‑type and Erbin‑knockout (Erbin‑/‑) mice, together with lipopolysaccharide (LPS)/adenosine triphosphate (ATP)‑stimulated bone marrow‑derived macrophages (BMDMs). Liver histopathology, mitochondrial ultrastructure, oxidative stress, inflammatory cytokine production, and pyroptosis‑related signaling were assessed using H&E staining, transmission electron microscopy, biochemical assays, ELISA, quantitative PCR, immunohistochemistry, and western blotting. Erbin deficiency markedly aggravated CLP‑induced liver injury, as evidenced by more severe histopathological damage, mitochondrial disruption, oxidative stress, NOD‑like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation, and pro‑inflammatory cytokine production. Mechanistically, Erbin deficiency promoted mitochondrial ROS accumulation, enhanced thioredoxin‑interacting protein (TXNIP)‑NLRP3 interactions, and intensified inflammatory activation and pyroptotic responses. Mitochondrial ROS scavenging with MitoQ substantially attenuated the pro‑pyroptotic and pro‑inflammatory effects of Erbin deficiency in LPS/ATP‑stimulated BMDMs. Collectively, these findings identify Erbin as an endogenous protective regulator that mitigates SLI by suppressing mitochondrial ROS‑driven TXNIP/NLRP3 inflammasome activation and inflammatory responses.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 6","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195206","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":" Leptin promotes obesity‑related osteoarthritis progression via CD44/JAK2/STAT3 axis‑mediated chondrocyte apoptosis.","authors":"Hao Qiu, Chao Zeng, Cheng Chen, Xin Zhou, Yongjun Zhu, Zhongliang Deng","doi":"10.3892/mmr.2026.14039","DOIUrl":"https://doi.org/10.3892/mmr.2026.14039","url":null,"abstract":"<p><p>Osteoarthritis (OA), especially obesity‑related OA, is a common joint disease in which leptin serves a notable role; however, the specific mechanism by which leptin promotes obesity‑related OA progression remains unclear. In the present study, human cartilage samples confirmed the association between leptin and obesity‑related OA. The Gene Expression Omnibus dataset GSE85785 was analyzed in R. Differential gene expression was screened using reverse transcription‑quantitative PCR. The protein levels of CD44, apoptosis‑related proteins and Janus kinase 2 (JAK2)/STAT3 pathway‑related proteins were examined using western blotting. Chondrocyte apoptosis was assessed using TUNEL staining and flow cytometry. Cartilage degeneration was evaluated using H&E and Safranin O‑Fast Green staining. Immunofluorescence staining and immunohistochemistry were employed to detect relevant proteins (Leptin, CD44, STAT3). The results from the present study demonstrated that leptin stimulation markedly upregulated CD44 expression, activated the JAK2/STAT3 signaling pathway and induced apoptosis in C28/I2 chondrocytes. Furthermore, the AG490 inhibitor markedly suppressed apoptosis. CD44 knockdown inhibited leptin‑induced activation of the JAK2/STAT3 pathway and apoptosis in C28/I2 chondrocytes, whereas CD44 overexpression activated JAK2/STAT3 signaling and promoted apoptosis. Animal experiments further confirmed that leptin administration induced OA, as shown by histological analysis (H&E and Safranin O‑Fast Green staining) revealing cartilage degeneration and matrix loss and TUNEL staining revealed increased chondrocyte apoptosis in leptin‑treated rats. In summary, the present study identified a novel mechanism by which leptin induced chondrocyte apoptosis and promoted OA through activation of the CD44‑mediated JAK2/STAT3 pathway.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"34 6","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149195209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"[Retracted] PYGB siRNA inhibits the cell proliferation of human osteosarcoma cell lines.","authors":"Shuwei Zhang, Yichi Zhou, Yuanyu Zha, Yang Yang, Linlong Wang, Jingfeng Li, Wei Jin","doi":"10.3892/mmr.2026.14014","DOIUrl":"10.3892/mmr.2026.14014","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 certain of the western blot data featured in Fig. 5A on p. 721 had already been published in an article in the journal <i>Experimental & Molecular Medicine</i> that was written by different authors at different research institutes, in addition to reappearing in other articles subsequently received and published in other journals that were also written by different authors at different research institutes. A subsequent investigation of this paper undertaken by the Editorial Office also revealed that flow cytometric data in Fig. 3A and B had already been published previously in other articles that were written by different authors at different research institutes, and the control GAPDH blots featured in Fig. 1B were strikingly similar to blots that were published in the years 2018‑2020 in three other articles written by different authors. Owing to the fact that the abovementioned data in this 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 satisfactory reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 18: 715‑722, 2018; DOI: 10.3892/mmr.2018.9022].</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/PMC13586801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945373","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":"Multi‑omics approaches to decipher the molecular mechanisms of exercise‑mediated bone protection: From mechanistic insights to personalized exercise prescription (Review).","authors":"Bin Tian, Xuesong Chen, Xin Kang","doi":"10.3892/mmr.2026.14009","DOIUrl":"10.3892/mmr.2026.14009","url":null,"abstract":"<p><p>The global burden of bone metabolic disorders necessitates a shift from generic exercise recommendations toward personalized prescription strategies. Exercise confers skeletal protection through mechanotransduction, yet the underlying molecular networks remain incompletely understood. Multi‑omics technologies, including transcriptomics, proteomics, metabolomics and single‑cell spatial approaches, have revolutionized the capacity to decode exercise‑mediated bone adaptation at the systems level. The present review synthesizes current single‑omics landscapes and integrative multi‑omics analyses that elucidate the core regulatory networks, mechanobiological coupling mechanisms and multiorgan crosstalk that are implicated in the bone response to mechanical loading. Translational applications across clinical scenarios such as osteoporosis, osteoarthritis and disuse bone loss are evaluated, and the technical, analytical and translational challenges limiting clinical implementation are addressed. Finally, the present review provides a framework for translating multi‑omics molecular signatures into personalized exercise prescriptions for optimized skeletal health.</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/PMC13579653/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891868","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] MicroRNA‑27a promotes tumorigenesis via targeting AKT in triple negative breast cancer.","authors":"Jing Wu, Zhihui Sun, Huijie Sun, Yanhua Li","doi":"10.3892/mmr.2026.14008","DOIUrl":"10.3892/mmr.2026.14008","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 certain of the cell migration and invasion data featured in Fig. 2C, G, H, K, L and O on p. 565‑6 were strikingly similar to data which appeared in a handful of other articles written by different authors at different research institutes, one of which had already been published in <i>Journal of Biological Research‑Thessaloniki</i> during the year before this paper was submitted to <i>Molecular Medicine Reports</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 17: 562‑570, 2018; DOI: 10.3892/mmr.2017.7886].</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/PMC13579645/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891919","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] Bcl11b regulates enamel matrix protein expression and dental epithelial cell differentiation during rat tooth development.","authors":"Ziyue Li, Guoqing Chen, Yaling Yang, Weihua Guo, Weidong Tian","doi":"10.3892/mmr.2026.14024","DOIUrl":"10.3892/mmr.2026.14024","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that, in the \"Protein extraction and western blotting\" subsection of the Materials and methods on p. 299, it was reported that 30 ng samples of protein were separated using SDS‑PAGE, a concentration that would be three orders of magnitude lower than what is typical. Furthermore, regarding the \"&lt;i&gt;Chromatin immunoprecipitation (ChIP) assay&lt;/i&gt;\" subsection of the Materials and methods on p. 298, the primer sequences described for targeting of the Msx2 promoter and the GAPDH control were identical to the sequences of the Msx2 and GAPDH primers reported in Table I, which were those used for RT‑qPCR analysis of cDNA derived from reverse‑transcribed mRNA. RT‑qPCR primers are designed to target exon sequences in cDNA, whereas ChIP primers are designed to target genomic promoter regions; therefore, these primers would not have been expected to have shared identical sequences, given that physically distinct genomic regions were being targeted. In their replies to these queries, the authors have confirmed that \"30 ng\" was a typo, and in the relevant subsection of the Materials and methods section, this should have been written as \"30 μg\". Concerning the nature of the primer sequences, the authors confirmed that the same GAPDH primer was in fact used as a negative primer control for both the ChIP and the RT‑qPCR analyses. However, the sequences used for the Msx gene for the RT‑qPCR analysis, as correctly presented in Table I, were inadvertently copied across to the \"&lt;i&gt;Chromatin immunoprecipitation (ChIP) assay&lt;/i&gt;\" subsection of the Materials and methods. In this section (p. 299, left‑hand column, sentence commencing on line 4), the sequences of these primers should have been written as follows (the changed primer sequences are highlighted in bold): \"Primers (forward AGT GCT GCA GTT GGT CAT TG and reverse CCT GCA AAT AAC GGG GTT CA) were used to amplify the Msx2 promoter\". The region from ‑1,200 to +100 bp relative to the Msx2 transcription start site (TSS) was selected as the sequence of interest. The RT‑PCR primers for GAPDH were used as control primers. In connection with the issue of presenting the correct sequences for the Msx gene for the RT‑qPCR analysis, the authors have realized that Fig. 4B was labeled incorrectly. As described in the Materials and methods and the Results sections, the ChIP assay was performed to detect the Msx2 promoter region, rather than the Bcl11b promoter. The labeling for the lanes of the gel in Fig. 4B has therefore been corrected to reflect this, and the revised version of Fig. 4 is shown on the next page. In addition, certain corrections were required to the legend for this figure, and the specific changes that have been made are highlighted as follows in bold: \"(B) PCR products of ChIP assay were verified by 2% agarose gel electrophoresis. Bcl11b, anti‑Bcl11b antibody; input, cell lysate; Positive control, anti‑RN","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/PMC13613962/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990481","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 progress of aptamers in the diagnosis and treatment of colorectal cancer (Review).","authors":"Yiwen Li, Penghui Yan, Ji Zhang, Binghui Wu, Min Li, Baoliang Bao","doi":"10.3892/mmr.2026.14012","DOIUrl":"10.3892/mmr.2026.14012","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is one of the leading causes of cancer‑related deaths. The high incidence rate and poor prognosis of CRC pose a serious threat to public health, and impose a notable social and economic burden. Therefore, improving the accuracy of the early diagnosis and treatment of CRC is of notable importance. Aptamers have substantial potential for tumor‑targeted diagnosis and treatment due to their unique advantages, such as high affinity, high specificity and programmability. In the diagnosis and treatment of CRC, aptamers can specifically target receptors on the surface of cancer cells and intervene in the development of CRC by inhibiting receptor activity. The present study reviews the current state of research on aptamers to provide a new scientific basis and methods for diagnosing and treating CRC. The relevant research achievements are organized based on the two major branches of diagnostic detection and targeted therapy to systematically assess the translational value of various CRC aptamers.</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/PMC13579126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945388","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 on the role and mechanism of SLC7A5 in idiopathic pulmonary fibrosis.","authors":"Menghan Wang, Yao Yu, Zhaoyu Liu, Dandan Xu, Yupeng Li, Xing Zou, Ning Shan, Xining Liu, Ce Shi, Hong Chen","doi":"10.3892/mmr.2026.14034","DOIUrl":"10.3892/mmr.2026.14034","url":null,"abstract":"<p><p>Idiopathic pulmonary fibrosis (IPF) is a progressive, chronic and fatal interstitial lung disease. The etiology of IPF remains to be fully elucidated and its prognosis remains poor with a short survival period. <i>Solute carrier family 7 member 5 (SLC7A5)</i> is an amino acid transporter that is responsible for the transportation of large neutral amino acids. The expression of SLC7A5 was found to be significantly upregulated in patients with IPF, as well as in the lung tissues of mice with bleomycin (BLM)‑induced pulmonary fibrosis and in human lung fibroblasts induced by transforming growth factor‑β1 (TGF‑β1). Both <i>SLC7A5</i> knockdown and the use of the selective <i>SLC7A5</i> inhibitor JPH203 affected the function of TGF‑β1‑induced myofibroblasts by inhibiting the PI3K/AKT/mTOR pathway. <i>In vivo</i>, JPH203 improved BLM‑induced pulmonary fibrosis in mice by inhibiting the activation of the PI3K/AKT/mTOR signaling pathway. Therefore, <i>SLC7A5</i> may represent a new therapeutic target for IPF. Future research should focus on therapeutic strategies regulating this target for translation into potential effective treatments for IPF in clinical practice.</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/PMC13659194/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149112166","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":"KIF4A drives esophageal squamous cell carcinoma via Wnt/β‑catenin signaling and predicts poor prognosis.","authors":"Jialong Chen, Tong Wang, Da Wang, Weiguo Liu, Chunlai Liu, Yang Yang, Xiangfu Sun, Lei Zhou","doi":"10.3892/mmr.2026.14013","DOIUrl":"10.3892/mmr.2026.14013","url":null,"abstract":"<p><p>Esophageal squamous cell carcinoma (ESCC) accounts for >90% of esophageal cancer cases in China, with a 5‑year overall survival rate of <30% for advanced disease. Kinesin family member 4A (KIF4A) is implicated in multiple malignancies; however, its functional mechanisms in ESCC remain incompletely elucidated. The present study investigated the prognostic value and tumor‑promoting mechanism of KIF4A in ESCC. KIF4A expression was detected in 43 paired ESCC and adjacent non‑malignant tissues, as well as in ESCC cell lines. Loss‑ and gain‑of‑function assays were performed to evaluate the effects of KIF4A on ESCC cell proliferation, migration and tumorigenesis <i>in vitro</i> and <i>in vivo</i>. RNA sequencing, co‑immunoprecipitation and rescue experiments were conducted to explore its downstream regulatory pathway. The results revealed that KIF4A was significantly upregulated in ESCC tissues and cell lines, and its high expression was closely associated with advanced tumor stage and poor overall survival in patients with ESCC. KIF4A knockdown markedly inhibited ESCC cell proliferation, migration and <i>in vivo</i> xenograft tumor growth, whereas its overexpression exerted opposite oncogenic effects. Mechanistically, KIF4A exerted tumor‑promoting effects by activating the canonical Wnt/β‑catenin signaling pathway via stabilization of the β‑catenin/T‑cell factor 7 complex. In conclusion, KIF4A may drive ESCC progression by activating the Wnt/β‑catenin signaling pathway, and may serve as a promising prognostic biomarker and therapeutic target for ESCC.</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/PMC13587026/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945445","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":"Arginine metabolism, polyamine homeostasis and ferroptosis in cancer: Molecular links and therapeutic opportunities (Review).","authors":"Xin Dong, Yongkun Hou, Jingjing Shao, Haixia Zhu, Jibin Liu","doi":"10.3892/mmr.2026.14022","DOIUrl":"10.3892/mmr.2026.14022","url":null,"abstract":"<p><p>Arginine metabolism, polyamine homeostasis and ferroptosis are interconnected molecular processes that influence tumor growth, immune remodeling and therapeutic responses. The availability of arginine is affected by tumor‑cell biosynthesis and uptake, myeloid arginase (ARG)‑mediated depletion, nitric oxide synthase (NOS)‑driven diversion and stromal‑vascular nutrient transport and microenvironmental remodeling. These input signals regulate the synthesis, uptake‑efflux cycling and catabolic turnover of polyamines, thereby creating an inhibitory buffering state or an oxidative state that can lower the ferroptosis threshold. Ferroptosis is controlled by the balance of lipid peroxidation triggers, including polyunsaturated fatty acid‑phospholipid load, iron‑dependent amplification and lipoxygenase activity, as well as buffering systems such as the cystine/glutamate antiporter system Xc-‑glutathione‑glutathione peroxidase 4 axis, ferroptosis suppressor protein 1‑coenzyme Q10, dihydroorotate dehydrogenase and GTP cyclohydrolase 1‑tetrahydrobiopterin (BH4). The immunological consequences of ferroptotic tumor‑cell death are context‑dependent, as dying cells may promote interferon‑gamma‑driven antitumor immunity or, conversely, reinforce myeloid‑mediated immunosuppression. The present review summarized the molecular links among arginine metabolism, polyamine homeostasis and ferroptosis in cancer and discusses therapeutic opportunities involving biomarker‑guided combinations targeting arginine, polyamine blockade, ferroptosis sensitization and immune checkpoint blockade.</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/PMC13601864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990465","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}