Molecular medicine reports最新文献

{"title":"Natural medicine‑empowered treatment of depression via restoring neurogenesis (Review).","authors":"Xiufen Zhong, Jingtao Gui","doi":"10.3892/mmr.2026.14002","DOIUrl":"10.3892/mmr.2026.14002","url":null,"abstract":"<p><p>Major depressive disorder (MDD) remains a leading cause of disability, with a substantial proportion of patients failing to achieve adequate remission following conventional monoaminergic antidepressant treatment. The present narrative review examines evidence primarily published between 2015 and 2025 concerning natural medicines, including phytochemicals, traditional formulations, marine‑derived products and dietary polyphenols, that may modulate neurogenesis relevant to depression. Adult hippocampal neurogenesis is regarded as one mechanistic framework rather than the sole explanation for depressive pathology. Priority was given to clinical and human‑derived evidence, while preclinical studies are employed to elucidate underlying mechanisms. Natural products appear to converge on pathways involving brain‑derived neurotrophic factor/tropomyosin receptor kinase B, Wnt/β‑catenin, NF‑κB/NLR family pyrin domain containing 3‑mediated immune regulation, autophagy, mitochondrial bioenergetics and the gut microbiota. Nevertheless, current clinical evidence remains insufficient to support the use of natural medicines as substitutes for established antidepressant therapies. Their most plausible near‑term application lies in standardized adjunctive or investigational interventions, pending larger biomarker‑stratified trials, rigorous safety assessment and optimized formulation strategies.</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/PMC13555594/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148840848","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] Coenzyme Q10 alleviates sevoflurane‑induced neuroinflammation by regulating the levels of apolipoprotein E and phosphorylated tau protein in mouse hippocampal neurons.","authors":"Man Yang, Naqi Lian, Yang Yu, Yaoqi Wang, Keliang Xie, Yonghao Yu","doi":"10.3892/mmr.2026.13995","DOIUrl":"10.3892/mmr.2026.13995","url":null,"abstract":"<p><p>Following the publication of the above article, a concerned author drew to the authors' attention that they had apparently used an inappropriate antibody in their study: In the Materials and methods section, the authors had reported the use of Abcam's recombinant antibody against plant homeodomain (PHD) finger protein 1 (a.k.a. PHF1; cat. no. ab184951) to probe for the unrelated protein, tau paired helical filaments (PHFs). The authors acknowledged that they had made a methodological error: They were intending to detect tau phosphorylation at Ser396/404, but mistakenly had used the antibody against PHD finger protein 1 (cat. no. ab184951; Abcam); as a result, the western blot results shown in Figs. 3 and  7 for protein PHF1 were invalid. This error went unnoticed since the two antibodies shared the same abbreviation (PHF1), and the banding patterns obtained with the incorrect antibody appeared similar in trend to what the authors had expected to have found, which unfortunately masked the mistake during their internal data review. The Editor instructed the authors to repeat the PHF1 western blot experiments using the correct PHF1 antibody (Tau‑pSer396/404; cat. no. 87061‑1‑RR; Proteintech Group, Inc.). The new experiments yielded reproducible and valid results, and the authors have replaced the original data relating to protein PHF1 in Figs. 3 and 7; the revised versions of these figures are shown on the next page. Note that these errors did not affect the results or the main conclusions reported in the study. All the authors approve of 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. The authors regret their oversight in selecting the wrong antibody for these specific western blot experiments, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 22: 445‑453, 2020; DOI: 10.3892/mmr.2020.11131].</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/PMC13504463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795544","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":"Role of microbial metabolites in the pathogenesis of hypertensive disorders of pregnancy: From short‑chain fatty acids to tryptophan metabolites (Review).","authors":"Fengyun Gao, Lili Wang, Guiyun Teng, Liqiong Shang","doi":"10.3892/mmr.2026.13981","DOIUrl":"10.3892/mmr.2026.13981","url":null,"abstract":"<p><p>Hypertensive disorders of pregnancy (HDP) are a leading cause of maternal and perinatal morbidity worldwide, and their pathogenesis involves complex interactions among vascular dysfunction, placental ischemia and immune dysregulation. The gut microbiota has been highlighted as a key upstream modulator, with microbial metabolites serving as key functional mediators rather than microbial composition alone. The present review focused on the roles of short‑chain fatty acids (SCFAs) and tryptophan metabolites in HDP pathogenesis. SCFAs and tryptophan‑derived metabolites modulate vascular function, immune tolerance and placental development via G protein‑coupled receptors, histone deacetylase inhibition and aryl hydrocarbon receptor (AhR) signaling. Their crosstalk underscores integrated regulatory networks at the maternal‑fetal interface. For example, butyrate promotes regulatory T cell differentiation via histone deacetylase inhibition, while indole‑3‑lactic acid activates the AhR; these pathways may synergistically enhance immune tolerance, yet competition for AhR binding between different tryptophan metabolites could produce antagonistic effects. Despite key progress, notable challenges remain regarding causal inference, methodological standardization and translational barriers. The present review aimed to synthesize current mechanistic insights and evaluate the clinical translation potential of targeting microbial metabolites for HDP prevention and management.</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/PMC13470050/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148685231","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":"Construction and validation of a nomogram for the diagnosis of postmenopausal osteoporosis.","authors":"Le-Yi Huang, Yao Chen, Lin-Ran Song, Zhuo-Lin Zhong, Kamran Ali, Hui-Min Li, Qing-Feng Hu, Hong-Hua Hu","doi":"10.3892/mmr.2026.13989","DOIUrl":"10.3892/mmr.2026.13989","url":null,"abstract":"<p><p>Osteoporosis (OP) is an increasing global public health concern and practical tools for predicting and detecting postmenopausal osteoporosis (PMOP) at an early stage are still needed. The present study aimed to develop and validate an individualized diagnostic prediction model for PMOP to facilitate risk assessment and guide therapeutic strategies for high‑risk patients. RNA sequencing data and corresponding clinical features were obtained from the Gene Expression Omnibus database (training group, n=90) and The Fourth Affiliated Hospital of School of Medicine and International School of Medicine, Zhejiang University, Zhejiang China (validation group, n=18). Gene Set Enrichment Analysis (GSEA) and Protein‑Protein Interaction (PPI) network analyses were used to identify hub genes associated with OP. Univariate, multivariate, least absolute shrinkage and selection operator logistic regression analyses were performed to identify the factors and generate a dynamic nomogram. Validation was performed using the receiver operating characteristic curve and decision curve analysis (DCA) to evaluate the effectiveness and net benefit of the clinical prediction nomogram. PPI and GSEA identified 13 estrogen‑response‑related hub genes (CD44, FDFT1, SLC29A1, P2RY2, RHOBTB3, TNNC1, RPS6KA2, TSKU, CYP26B1, SEMA3B, SYT12, IL17RB and ELF3) that were incorporated into a risk score model. A nomogram combining this risk score with clinical parameters demonstrated a promising preliminary diagnostic performance for OP. DCA indicated that the combined risk score and clinical‑factor model provided the highest net benefit. The clinical prediction nomogram exhibited a promising preliminary performance in both the training and validation groups. The present study developed a novel diagnostic nomogram for predicting PMOP. This exploratory tool showed potential clinical utility for risk stratification, although prospective validation in larger cohorts is required before clinical application.</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/PMC13501392/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148762289","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":"Inhibition of Dyrk1a attenuates type 1 diabetic cardiomyopathy via anti‑ferroptosis.","authors":"Junjian Chen, Wanyi Zhang, Tao Hong, Junsheng Wang, Chuan Chen, Ying Zhang, Mi Hu, Ning You, Jietao Huang","doi":"10.3892/mmr.2026.13996","DOIUrl":"10.3892/mmr.2026.13996","url":null,"abstract":"<p><p>Diabetic cardiomyopathy (DCM) is a major complication of type 1 diabetes mellitus (T1DM) with limited treatment options. Dyrk1a is involved in multiple diseases, comprising neurodegenerative disorders, cancer and diabetes. In addition, Dyrk1a is an emerging therapeutic target. Nonetheless, it remains ambiguous with regard to its role in T1DM‑related DCM. The present study investigated the function and mechanisms of Dyrk1a in DCM. Experimental T1DM was induced through sequential low‑dose streptozotocin administrations via intraperitoneal delivery. The investigation showed conspicuous cardiac upregulation of Dyrk1a protein expression in this T1DM murine model. Pharmacological intervention was performed by employing the Dyrk1a‑targeting compound harmine, administered through oral gavage, which ameliorated cardiac dysfunction characteristic of DCM. This therapeutic efficacy was mechanistically linked to ferroptosis inhibition, which was established through harmine‑mediated attenuation of pathological signatures, namely reduced malondialdehyde accumulation, enhanced glutathione bioavailability, as well as elevated expression of ferroptosis regulators SLC7A11 and GPX4. It is noteworthy that co‑administration of the ferroptosis activator erastin nullified the cardioprotective properties of harmine. Together, these findings establish harmine as an effective modulator of ferroptosis pathways, conferring protection against hyperglycemia‑induced cardiomyocyte injury. Dyrk1a inhibition enhances cardiac function in T1DM by reducing ferroptosis.</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/PMC13504439/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795556","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":"UBE2A as a prognostic indicator across human cancers: Insights from multi‑omics and immune landscape analyses.","authors":"Yun Wen, Pengfei Luo","doi":"10.3892/mmr.2026.13970","DOIUrl":"10.3892/mmr.2026.13970","url":null,"abstract":"<p><p>Ubiquitin‑conjugating enzyme E2A (UBE2A), a member of the ubiquitin‑conjugating E2 enzyme family, has been implicated in tumor development; however, its role across human cancer types remains incompletely understood. The present study aimed to systematically characterize the expression pattern, prognostic importance and immune relevance of UBE2A in a pan‑cancer context. Public datasets, including The Cancer Genome Atlas, Gene Expression Omnibus and Genotype‑Tissue Expression, were integrated to evaluate UBE2A expression, clinical importance, molecular characteristics, immune associations and biological functions across cancer types. Single‑cell RNA sequencing data were analyzed to investigate the cellular distribution of UBE2A. Functional validation was performed through UBE2A knockdown in breast cancer cell lines. Results indicated that UBE2A was significantly upregulated in a number of cancer types and was associated with unfavorable overall and progression‑free survival. UBE2A expression exhibited significant correlations with immune cell infiltration and immune checkpoint‑associated genes across cancer types. Functional enrichment analyses indicated that UBE2A was primarily involved in cell cycle regulation and proliferative processes. Single‑cell analysis revealed preferential UBE2A expression in proliferative T‑cell populations. Furthermore, <i>in vitro</i> experiments demonstrated that UBE2A knockdown significantly suppressed breast cancer cell proliferation, migration and invasion. Overall, UBE2A was shown to be a promising prognostic biomarker associated with tumor progression, cell cycle activity and immune‑associated characteristics across cancer types. Its preferential expression in proliferative T‑cell populations and oncogenic role in breast cancer suggest that UBE2A may serve as a potential therapeutic target and a candidate biomarker for evaluating tumor prognosis and the tumor immune microenvironment.</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/PMC13443290/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148579397","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] MicroRNA‑145‑5p suppresses fascin to inhibit the invasion and migration of cervical carcinoma cells.","authors":"Shufang He, Guiyuan Yu, Ke Peng, Sisun Liu","doi":"10.3892/mmr.2026.13988","DOIUrl":"10.3892/mmr.2026.13988","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that the Transwell migration and invasion assay experiments shown in Figs. 3D, 6D and F, and 7G and I contained three sets of overlapping sections of data, such that data which were intended to show the results of differently performed experiments had apparently been derived from the same original sources. In addition, the 'si‑FSCN1' data panel for the migration assay experiments shown in Fig. 6D apparently reappeared in Fig. 6 of another paper written by different authors at different research institutes, which was submitted at a later date to the journal <i>Medical Science Monitor</i>. The authors have been contacted by the Editorial Office to offer an explanation for the apparent anomalies in the presentation of the data in this paper, and we are awaiting their response. Owing to the fact that the Editorial Office has 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 22: 5282‑5292, 2020; DOI: 10.3892/mmr.2020.11592].</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/PMC13494849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148764887","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] PPM1A as a key target of the application of Jiawei‑Maxing‑Shigan decoction for the attenuation of radiation‑induced epithelial‑mesenchymal transition in type II alveolar epithelial cells.","authors":"Jinhua Lu, Shengyou Lin, Zechen Lin, Xianlei Lin, Yuezhong Shen, Jingyang Su","doi":"10.3892/mmr.2026.13971","DOIUrl":"10.3892/mmr.2026.13971","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 Figs. 2B, 4B, 5C and 6A had either already been submitted for publication, or were already published, in several articles in different journals written by different authors at different research institutes. A subsequent investigation of this paper underaken by the Editorial Office confirmed the authenticity of these findings. Owing to the fact that the contentious data in the above article had either already been submitted for publication, or were already 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 24: 825, 2021; DOI: 10.3892/mmr.2021.12465].</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/PMC13439036/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630846","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":"From oxidative stress to epigenetic regulation: Molecular mechanisms of preterm brain injury and neuroprotective strategies (Review).","authors":"Yuying Li, Ling Wei, Fang Sun, Huixia Wu, Xijun Sun, Yirong Gan, Xiaohua Kong","doi":"10.3892/mmr.2026.14005","DOIUrl":"10.3892/mmr.2026.14005","url":null,"abstract":"<p><p>Preterm brain injury remains a leading cause of long‑term neurodevelopmental impairment despite advances in neonatal care. Oxidative stress (OS), arising from mitochondrial dysfunction, nicotinamide adenine dinucleotide phosphate oxidase activation and iron‑mediated Fenton reactions, selectively damages the developing brain because of immature antioxidant defenses and vulnerable oligodendrocyte progenitor cells. Critically, OS triggers enduring epigenetic modifications including DNA methylation alterations, histone acetylation changes and microRNA dysregulation, thereby translating acute perinatal insults into sustained changes in gene expression. The complex cellular interplay involving microglia, astrocytes and the neurovascular unit determines injury progression and repair capacity. Emerging neuroprotective strategies include antioxidant therapies, pathway‑targeted agents and cell‑based approaches, while artificial intelligence applications show promise for early risk stratification and personalized monitoring, although these tools remain under prospective validation. The present review synthesized current evidence on the pathological cascade from OS to epigenetic dysregulation in preterm brain injury, evaluated the latest advances in neuroprotective interventions and aimed to inform the development of precision‑based, developmentally timed interventions that address the multifactorial nature of preterm brain injury and improve long‑term neurodevelopmental outcomes.</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/PMC13573286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148891752","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":"Role of CMTM6 in disease pathogenesis and clinical translation potential (Review).","authors":"Rongtou Huang, Danning Mo, Huitian Huang, Minmin Zhang, Wenhong Yu, Buqing Cao","doi":"10.3892/mmr.2026.13977","DOIUrl":"10.3892/mmr.2026.13977","url":null,"abstract":"<p><p>The chemokine‑like factor (CKLF)‑like MARVEL transmembrane domain‑containing (CMTM) family belongs to the human CKLF gene superfamily, which comprises CKLF and CMTM1‑8. Among its members, CMTM6 encodes a protein exhibiting structural and functional characteristics that lie between classical chemokines and tetraspanins. CMTM6 is expressed in several normal tissues, including those of the immune, reproductive and nervous systems. Notably, its expression is frequently upregulated across a broad spectrum of tumors including, but not limited to, carcinomas of the lung, liver and gastrointestinal tract. CMTM6 contributes to tumor proliferation, invasion and metastasis by inhibiting immune responses, facilitating immune evasion and inducing epithelial‑mesenchymal transition, thereby influencing patient prognosis and survival outcomes. The present review systematically summarizes the molecular functions, mechanisms of action, disease‑related expression patterns and clinical translational applications of CMTM6, aiming to provide novel clinical insights and to guide the development of CMTM6‑targeted therapeutic strategies.</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/PMC13454919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148630888","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}