Expert Reviews in Molecular Medicine最新文献

{"title":"Modulation of Female Reproductive Functions through Nerve Growth Factor: A Systematic Review.","authors":"Yanru Lou, Shuo Huang, Xi Zhang, Wei Guo, Lina Yi, Leihan Wang, Shuangyi Gong, Jie Yan, Rui Yang","doi":"10.1017/erm.2026.10050","DOIUrl":"https://doi.org/10.1017/erm.2026.10050","url":null,"abstract":"","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":" ","pages":"1-19"},"PeriodicalIF":5.5,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147845641","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of acupuncture in women with polycystic ovary syndrome undergoing in vitro fertilization: a systematic review and Meta-analysis.","authors":"Lina Yi, Haolin Zhang, Tian Tian, Yaodong Zhang, Yanru Lou, Jialin Li, Chenhong Liu, Caihong Ma, Ping Liu, Rong Li, Jie Qiao, Shuo Huang, Rui Yang","doi":"10.1017/erm.2026.10048","DOIUrl":"https://doi.org/10.1017/erm.2026.10048","url":null,"abstract":"","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":" ","pages":"1-25"},"PeriodicalIF":5.5,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147823088","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obesity-Related Cognitive Impairment: An update overview of mechanisms and treatments.","authors":"Chuanyu Zhong, Kai Chen, Shu Lin, Yinqiong Huang","doi":"10.1017/erm.2026.10049","DOIUrl":"https://doi.org/10.1017/erm.2026.10049","url":null,"abstract":"","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":" ","pages":"1-37"},"PeriodicalIF":5.5,"publicationDate":"2026-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147823043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When GPVI Goes Rogue: Pathogenesis and Therapeutic Horizons in ITP.","authors":"Jalal Naghinezhad, Ahmad Mohajerian, Shana Ahadi, Nastaran Khodakarim, Michael R Hamblin, Hadi Rezaeeyan","doi":"10.1017/erm.2026.10047","DOIUrl":"https://doi.org/10.1017/erm.2026.10047","url":null,"abstract":"","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":" ","pages":"1-41"},"PeriodicalIF":5.5,"publicationDate":"2026-04-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147678576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Tumor-Platelet-Immune Interface: Driving Metastasis, Pre-Metastatic Niche Formation, and Therapeutic Vulnerabilities.","authors":"Jalal Naghinezhad, Ehsan Kamali Yazdi, Ahmad Mohajerian, Negin Yousefi Chermehini, Pedram Ghanavati, Hamid Motamedi, Hadi Rezaeeyan","doi":"10.1017/erm.2026.10043","DOIUrl":"https://doi.org/10.1017/erm.2026.10043","url":null,"abstract":"","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":" ","pages":"1-34"},"PeriodicalIF":5.5,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147628671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beyond Antibiotics: Alternative Strategies Targeting <i>Helicobacter pylori</i> Resistance.","authors":"Amin Fath Tabar, Azar Nejati, Seyedeh Nasim Mirbahari, Mohammad Rahmanian, Ehsan Nazemalhosseini Mojarad, Zahra Sadeghloo, Hamideh Raeisi","doi":"10.1017/erm.2026.10040","DOIUrl":"10.1017/erm.2026.10040","url":null,"abstract":"<p><p>The escalating global prevalence of antibiotic-resistant <i>Helicobacter pylori</i> strains has undermined conventional eradication therapies, heightening the burden of associated conditions such as gastritis, peptic ulcers and gastric malignancies. Emerging non-antibiotic alternatives, including natural and synthetic compounds, probiotics and vaccine candidates, offer potential solutions to combat these infections effectively. Natural and synthetic compounds provide promising anti-<i>H. pylori</i> effects, primarily through bacterial membrane disruption, urease inhibition, virulence gene suppression and biofilm prevention. in vitro and in vivo studies support the robust activity of natural agents, while synthetic counterparts demonstrate potent bactericidal and anti-adherence capabilities, though rigorous clinical validation is still required. Probiotic strains enhance eradication rates when combined with antibiotics, reduce treatment-related adverse effects, modulate gut microbiota and attenuate gastric inflammation and carcinogenesis. Vaccine development encompasses whole-cell, subunit and DNA platforms targeting key virulence factors, showing immunogenicity and protective efficacy in preclinical models, yet is limited by variable clinical translation and insufficient large-scale trials. Despite promising advancements, challenges persist, including inconsistent efficacy and a need for more rigorous human studies. Future efforts should emphasize combinatorial therapies, refined delivery systems, and thorough safety evaluations to integrate these strategies into clinical practice, fostering sustainable management of <i>H. pylori</i> in a post-antibiotic era.</p>","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":" ","pages":"e18"},"PeriodicalIF":5.5,"publicationDate":"2026-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147628649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From lactate to lactylation: novel pathological mechanisms and potential therapeutic targets for high-altitude cerebral oedema.","authors":"Chaoyi Duan, Siyu Li, Likun Yao, Xinjie Zhang, Yansheng Ding, BiWen Peng","doi":"10.1017/erm.2026.10046","DOIUrl":"10.1017/erm.2026.10046","url":null,"abstract":"<p><strong>Background: </strong>High altitude cerebral edema (HACE), a fatal terminal stage of acute mountain sickness (AMS), is triggered by rapid exposure to hypoxia at high altitudes. The pathophysiology of HACE is complex, involving multiple key processes including energy metabolism disorders, oxidative stress, blood-brain barrier (BBB) injury, and neuroinflammation, all of which interact to drive disease progression. Lactylation, a novel epigenetic regulatory mechanism discovered in 2019, provides a fresh perspective for HACE research.</p><p><strong>Methods: </strong>This study integrates the latest research findings on the pathophysiology of HACE, lactate metabolism, and the role of lactylation in hypoxia-related diseases (such as cancer and ischemic-hypoxic diseases). It focuses on analyzing the potential molecular mechanisms of lactylation in HACE, including its regulation of the HIF-1α/NF-κB axis, inflammation, and metabolism, and discusses existing lactylation regulation strategies.</p><p><strong>Results: </strong>In HACE, hypoxia-driven glycolysis elevates lactate, promoting protein lactylation (e.g., NuRD complex in microglia, which is correlated with proinflammatory cytokines). Lactylation may regulate HIF-1α/NF-κB axis, inflammation, and metabolism in HACE pathogenesis. Currently, methods such as the inhibition of lactate dehydrogenase (LDH) /monocarboxylate transporters and the use of histone deacetylase inhibitors have been proven effective in regulating lactylation.</p><p><strong>Conclusion: </strong>Lactylation is a key link connecting metabolic disorders and neuroinflammation in HACE. However, the dual role of lactate in neuroprotection and neuroinjury under hypoxic conditions still requires further exploration. Future research should focus on deciphering the molecular networks related to HACE and developing precise intervention strategies to provide new directions for HACE treatment.</p>","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":" ","pages":"e16"},"PeriodicalIF":5.5,"publicationDate":"2026-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13148425/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147624474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxeiptosis - potential in cancer treatment?","authors":"Mateusz Kciuk, Katarzyna Wanke, Żaneta Kałuzińska-Kołat, Renata Kontek","doi":"10.1017/erm.2026.10045","DOIUrl":"10.1017/erm.2026.10045","url":null,"abstract":"<p><p>Oxeiptosis is a reactive oxygen species (ROS)-dependent form of programmed cell death that plays a key role in cellular homeostasis and holds promise as a cancer therapy. This review explores its molecular mechanisms, emphasizing the KEAP1-PGAM5-AIFM1 signalling pathway and its reliance on ROS accumulation. Compared to other cell death pathways, oxeiptosis offers a distinct approach, especially for targeting cancer cells resistant to conventional therapies. The review evaluates emerging inducers, both synthetic and natural, that selectively trigger oxeiptosis in cancer cells. It also examines the potential synergy between oxeiptosis and ROS-generating chemotherapies, particularly in the oxidative tumour microenvironment. However, challenges remain, including identifying tumour-specific inducers, overcoming cancer cell resistance to oxidative stress and reducing off-target effects. The review concludes by highlighting the need for targeted delivery strategies and rigorous preclinical studies to translate oxeiptosis into effective cancer treatments. Overall, it underscores oxeiptosis as a promising avenue to address drug resistance and improve therapeutic outcomes in oncology.</p>","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":" ","pages":"e15"},"PeriodicalIF":5.5,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13148423/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147522672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia and HIF signalling in tumour microenvironment: linking immune evasion, metabolic rewiring and epigenetic regulation.","authors":"Shadiya Fawzul Ameer, Elham Abdul Latif M Sharif, Wisam Nabeel Ibrahim","doi":"10.1017/erm.2026.10044","DOIUrl":"10.1017/erm.2026.10044","url":null,"abstract":"<p><strong>Background: </strong>Hypoxia is a defining feature of the tumour microenvironment (TME) that drives aggressive tumour behaviour through coordinated adaptive responses. Hypoxia-inducible factors (HIFs), particularly HIF-1α, play a central role in orchestrating metabolic, immune and epigenetic reprogramming within tumours.</p><p><strong>Objective: </strong>This review aims to elucidate the integrated roles of hypoxia in regulating angiogenesis, immune suppression, metabolic adaptation and epigenetic modifications, and to highlight their collective impact on tumour progression and therapeutic resistance.</p><p><strong>Methods: </strong>A comprehensive review of current literature was conducted to examine the molecular and cellular mechanisms mediated by hypoxia and HIF signalling within the TME, with a focus on their interplay across angiogenic, immune, metabolic and epigenetic pathways.</p><p><strong>Results: </strong>HIF-1α promotes the expression of pro-angiogenic factors, including VEGF, ANGPT2 and CXCL12, leading to abnormal vascularisation and recruitment of immunosuppressive cells such as regulatory T cells and myeloid-derived suppressor cells. This disorganised vasculature exacerbates hypoxia, reinforcing a cycle of immune evasion and metabolic stress. Hypoxia also upregulates immune checkpoint molecules (e.g., PD-L1, PD-1), contributing to T-cell exhaustion and impaired dendritic cell function. Concurrently, metabolic reprogramming-characterised by increased glycolysis, lactate accumulation and extracellular acidification-suppresses cytotoxic T cell and NK cell activity. Epigenetic regulators, including histone demethylases and DNA methyltransferases, sustain these adaptations through persistent transcriptional changes, referred to as hypoxic memory.</p><p><strong>Conclusion: </strong>Hypoxia acts as a central organising force within the TME, coordinating angiogenic, immune, metabolic and epigenetic processes to promote tumour progression. Targeting HIF-driven pathways represents a promising therapeutic strategy to overcome immune resistance, enhance drug delivery and improve the efficacy of combination treatments, including immunotherapy and metabolic interventions. This review underscores the importance of integrated approaches to disrupt hypoxia-mediated tumour adaptation.</p>","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":" ","pages":"e14"},"PeriodicalIF":5.5,"publicationDate":"2026-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13148424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147522654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting JAK/STAT Signaling with Cold Atmospheric Plasma: A Potential Therapy for Systemic Lupus Erythematosus.","authors":"Xiaofeng Dai, Yuting Fan","doi":"10.1017/erm.2026.10042","DOIUrl":"https://doi.org/10.1017/erm.2026.10042","url":null,"abstract":"","PeriodicalId":50462,"journal":{"name":"Expert Reviews in Molecular Medicine","volume":" ","pages":"1-32"},"PeriodicalIF":5.5,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147505463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}