Pub Date : 2026-02-02DOI: 10.1007/s43032-025-02015-1
Ying Chen, Yi Zhang, Qinyin Deng, Nan Shan, Wei Peng, Xin Luo, Hua Zhang, Philip N Baker, Chao Tong, Hongbo Qi
{"title":"Correction: Inhibition of Wnt Inhibitory Factor 1 Under Hypoxic Condition in Human Umbilical Vein Endothelial Cells Promoted Angiogenesis in Vitro.","authors":"Ying Chen, Yi Zhang, Qinyin Deng, Nan Shan, Wei Peng, Xin Luo, Hua Zhang, Philip N Baker, Chao Tong, Hongbo Qi","doi":"10.1007/s43032-025-02015-1","DOIUrl":"https://doi.org/10.1007/s43032-025-02015-1","url":null,"abstract":"","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146106919","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}
Pub Date : 2026-02-02DOI: 10.1007/s43032-025-02034-y
Ana Claudia M Scalioni, Luciana Bastos-Rodrigues, Elaine Sousa, Tays F Guedes, André L Caldeira-Brant, Luiz De Marco, Wiviane A Assis, Fernando M Reis
{"title":"Fibrosis Severity and Pro-fibrotic Gene Expression in Uterine Leiomyomas: Relationship with Self-reported Skin Color/Race and Genomic Ancestry.","authors":"Ana Claudia M Scalioni, Luciana Bastos-Rodrigues, Elaine Sousa, Tays F Guedes, André L Caldeira-Brant, Luiz De Marco, Wiviane A Assis, Fernando M Reis","doi":"10.1007/s43032-025-02034-y","DOIUrl":"https://doi.org/10.1007/s43032-025-02034-y","url":null,"abstract":"","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146106921","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}
Pub Date : 2026-01-22DOI: 10.1007/s43032-025-02021-3
Vittorio Unfer, Maria Luisa Casini, Loredana Costabile, Marcella Mignosa, Sandro Gerli, Gian Carlo Di Renzo
{"title":"Retraction Note To: High Dose of Phytoestrogens Can Reverse the Antiestrogenic Effects of Clomiphene Citrate on the Endometrium in Patients Undergoing Intrauterine Insemination: A Randomized Trial.","authors":"Vittorio Unfer, Maria Luisa Casini, Loredana Costabile, Marcella Mignosa, Sandro Gerli, Gian Carlo Di Renzo","doi":"10.1007/s43032-025-02021-3","DOIUrl":"https://doi.org/10.1007/s43032-025-02021-3","url":null,"abstract":"","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146030562","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}
Pub Date : 2026-01-21DOI: 10.1007/s43032-026-02053-3
Daoyang Zou, Xiuhong Wu, Xi Xin, Tianwen Xu
{"title":"Correction to: Construction and Validation of a Novel Prognostic Model Based on Cervical Cancer-Related Genes.","authors":"Daoyang Zou, Xiuhong Wu, Xi Xin, Tianwen Xu","doi":"10.1007/s43032-026-02053-3","DOIUrl":"https://doi.org/10.1007/s43032-026-02053-3","url":null,"abstract":"","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146019478","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}
Pub Date : 2026-01-21DOI: 10.1007/s43032-025-02033-z
Fateme Arjmand, Jamileh Sadat Mirsanei, Rana Mehdizadeh, Mehdi Mehdizadeh
Primary ovarian insufficiency (POI) is a multifactorial disorder marked by ovarian function cessation before age 40, leading to infertility and systemic complications, including osteoporosis, cardiovascular disease, and neurocognitive impairment. It results from accelerated ovarian reserve depletion, impaired folliculogenesis, and hormonal dysregulation. The majority of cases are idiopathic, with known causes including genetic mutations, autoimmune disorders, infections, and iatrogenic factors. Recent RNA sequencing advances highlight microRNAs (miRNAs) as critical regulators of ovarian processes. Dysregulated miRNAs drive granulosa cell apoptosis, oxidative stress, and follicular atresia, with distinct profiles offering potential as biomarkers for early diagnosis and therapeutic targets. This review synthesizes miRNA-mediated mechanisms in POI, integrating their roles in apoptosis, DNA repair, and folliculogenesis, and evaluates miRNA-based diagnostics and therapies, including exosome-mediated delivery, to improve reproductive and clinical outcomes.
{"title":"Primary Ovarian Insufficiency: Molecular Mechanisms and the Role of MicroRNAs.","authors":"Fateme Arjmand, Jamileh Sadat Mirsanei, Rana Mehdizadeh, Mehdi Mehdizadeh","doi":"10.1007/s43032-025-02033-z","DOIUrl":"https://doi.org/10.1007/s43032-025-02033-z","url":null,"abstract":"<p><p>Primary ovarian insufficiency (POI) is a multifactorial disorder marked by ovarian function cessation before age 40, leading to infertility and systemic complications, including osteoporosis, cardiovascular disease, and neurocognitive impairment. It results from accelerated ovarian reserve depletion, impaired folliculogenesis, and hormonal dysregulation. The majority of cases are idiopathic, with known causes including genetic mutations, autoimmune disorders, infections, and iatrogenic factors. Recent RNA sequencing advances highlight microRNAs (miRNAs) as critical regulators of ovarian processes. Dysregulated miRNAs drive granulosa cell apoptosis, oxidative stress, and follicular atresia, with distinct profiles offering potential as biomarkers for early diagnosis and therapeutic targets. This review synthesizes miRNA-mediated mechanisms in POI, integrating their roles in apoptosis, DNA repair, and folliculogenesis, and evaluates miRNA-based diagnostics and therapies, including exosome-mediated delivery, to improve reproductive and clinical outcomes.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146019408","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}
Human papillomavirus (HPV) and Chlamydia trachomatis (CT) co-infection is increasingly recognized not as a mere coincidence, but as a synergistic partnership that accelerates oncogenic progression across multiple tissues. This review synthesizes existing evidence into a "central-peripheral" framework, positioning cervical cancer as the central, mechanistically well-established model of cooperation, while malignancies such as head and neck, ovarian, and breast cancers represent the emerging, though less substantiated, peripheral extensions. This synthesis delineates an emerging paradigm of bidirectional interplay: CT fosters a permissive microenvironment for HPV persistence by impairing host immunity and inducing chronic inflammation, while HPV oncoproteins promote tumorigenesis by disrupting tumor suppressor functions and reprogramming cellular metabolism. These resulting metabolic alterations in the host cell form the basis for the hypothesis of a metabolic co-dependency that may further reinforce CT persistence. The convergence of these pathogens on shared pathways, specifically immune evasion, genomic instability, and metabolic reprogramming, outlines a synergistic network. However, definitive proof of causality, particularly for the bidirectional effects in non-cervical cancers, remains constrained by methodological heterogeneity. Bridging these gaps requires future research to leverage immunocompetent co-infection models and multi-omics approaches. Elucidating the HPV-CT interactome supports a conceptual shift from a single-pathogen to a multi-pathogen oncogenesis model, which is pivotal for developing the next generation of precision prevention and therapy.
{"title":"Synergism on Cancer Development of Human Papillomavirus and Chlamydia Trachomatis Co-Infection.","authors":"Erqun Tang, Yaqi Liao, Zhenlei Wang, Lanhua Zhao, Mingxia Yang, Youjun Chen, Shuangyang Tang","doi":"10.1007/s43032-025-02042-y","DOIUrl":"https://doi.org/10.1007/s43032-025-02042-y","url":null,"abstract":"<p><p>Human papillomavirus (HPV) and Chlamydia trachomatis (CT) co-infection is increasingly recognized not as a mere coincidence, but as a synergistic partnership that accelerates oncogenic progression across multiple tissues. This review synthesizes existing evidence into a \"central-peripheral\" framework, positioning cervical cancer as the central, mechanistically well-established model of cooperation, while malignancies such as head and neck, ovarian, and breast cancers represent the emerging, though less substantiated, peripheral extensions. This synthesis delineates an emerging paradigm of bidirectional interplay: CT fosters a permissive microenvironment for HPV persistence by impairing host immunity and inducing chronic inflammation, while HPV oncoproteins promote tumorigenesis by disrupting tumor suppressor functions and reprogramming cellular metabolism. These resulting metabolic alterations in the host cell form the basis for the hypothesis of a metabolic co-dependency that may further reinforce CT persistence. The convergence of these pathogens on shared pathways, specifically immune evasion, genomic instability, and metabolic reprogramming, outlines a synergistic network. However, definitive proof of causality, particularly for the bidirectional effects in non-cervical cancers, remains constrained by methodological heterogeneity. Bridging these gaps requires future research to leverage immunocompetent co-infection models and multi-omics approaches. Elucidating the HPV-CT interactome supports a conceptual shift from a single-pathogen to a multi-pathogen oncogenesis model, which is pivotal for developing the next generation of precision prevention and therapy.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146012133","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":"Female Infertility and Risk for Later-Life Cardiovascular Disease: Lessons from a Mouse Model of Human Cardiovascular Disease.","authors":"Ayaka Tanaka, Hitomi Nakamura, Namhyo Kim, Hajime Nakaoka, Makoto Nishida, Keiichi Kumasawa, Yasushi Sakata, Shizuya Yamashita, Tadashi Kimura","doi":"10.1007/s43032-025-02026-y","DOIUrl":"https://doi.org/10.1007/s43032-025-02026-y","url":null,"abstract":"","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145989816","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}
Oligoasthenozoospermia (OAT) is a major cause of declining male fertility worldwide, characterized by reduced sperm count and motility. Its pathogenesis involves multiple factors including genetics, hormones, environment, and lifestyle. Due to ethical and practical limitations in human studies, animal models have become essential tools for elucidating OAT mechanisms and evaluating therapeutic strategies. This review aims to systematically organize and evaluate existing OAT animal models, including those established through chemical agents, heavy metals, endocrine disruptors, physical stress, genetic modification, and nutritional imbalance. It summarizes these models based on their mechanistic foundations, phenotypic characteristics, advantages, and limitations. Results indicate that despite significant research advances, existing models remain limited in standardization, depth of mechanism elucidation, and clinical translational value. Therefore, future efforts should focus on developing more comprehensive and clinically relevant animal models to deepen understanding of OAT pathophysiology and advance the development of effective and personalized therapeutic strategies.
{"title":"Advances in Research on Models of Oligoasthenozoospermia.","authors":"Feng Yang, Yongyong Ren, Junpeng Zhang, Changli Wang, Meng Sun, Jin Li, Anqi Geng","doi":"10.1007/s43032-025-02019-x","DOIUrl":"https://doi.org/10.1007/s43032-025-02019-x","url":null,"abstract":"<p><p>Oligoasthenozoospermia (OAT) is a major cause of declining male fertility worldwide, characterized by reduced sperm count and motility. Its pathogenesis involves multiple factors including genetics, hormones, environment, and lifestyle. Due to ethical and practical limitations in human studies, animal models have become essential tools for elucidating OAT mechanisms and evaluating therapeutic strategies. This review aims to systematically organize and evaluate existing OAT animal models, including those established through chemical agents, heavy metals, endocrine disruptors, physical stress, genetic modification, and nutritional imbalance. It summarizes these models based on their mechanistic foundations, phenotypic characteristics, advantages, and limitations. Results indicate that despite significant research advances, existing models remain limited in standardization, depth of mechanism elucidation, and clinical translational value. Therefore, future efforts should focus on developing more comprehensive and clinically relevant animal models to deepen understanding of OAT pathophysiology and advance the development of effective and personalized therapeutic strategies.</p>","PeriodicalId":20920,"journal":{"name":"Reproductive Sciences","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145966737","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}