Reproductive Sciences生殖科学
Reproductive Sciences(英文缩写 REPROD SCI),ISSN 1933-7191,eISSN 1933-7205,中文译名:生殖科学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-10-01 至 2026-09-30，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 2.924 | Q3 |
| 2022 | 2.900 | Q2 |
| 2023 | 2.600 | Q2 |
| 2024 | 2.500 | Q2 |
| 2025 | 2.800 | Q2 |
Reproductive Sciences 最新收录文献
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1. The Building and Application of a Machine Learning Model on Predicting Euploid Blastocysts in IVF Treatments Without PGT-A.
PMID:日期:2026-10-02Embryologists could not know whether blastocysts were euploid or not in in-vitro fertilization treatments without preimplantation genetic testing for aneuploidy. However, preimplantation genetic testing for aneuploidy technology which might impair the developmental potency of blastocysts was in strict limitation in China. Therefore, a non-invasive method was necessary for embryologists to select euploid embryos as far as possible. A machine learning model based on preimplantation genetic testing for aneuploidy results, development dynamics, morphology of blastocysts and female age was built by two-logistic regression analysis. The area under the receiver operating characteristic curve of the model was 0.877. The accuracy rate, precision rate, recall rate, f-score, true negative rate, false positive rate, false negative rate of the model when performed in independent data set were 77.35%, 77.49%, 72.55%, 74.94%, 81.55%, 18.45%, 27.45%, respectively. Besides, the false positive rate of the model on predicting euploid blastocysts was significantly lower than Gardner grade and KIDScore D5. When selected blastocysts by the model, the frozen embryo transfer outcomes improved significantly than the frozen embryo transfer outcomes which selected blastocysts by Gardner selection. The predictive model had potency in selecting euploid blastocysts in in-vitro fertilization treatments without preimplantation genetic testing for aneuploidy technology.
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2. TRIP10 as a Key Regulator in Fetal Growth Restriction: a Study Integrating Bioinformatics Screening with Experimental Validation.
PMID:日期:2026-10-01Fetal growth restriction (FGR) is a leading cause of perinatal mortality, yet its molecular mechanisms remain poorly understood. This study integrated bioinformatic analysis with experimental validation to identify key genes involved in FGR pathogenesis. Transcriptome datasets GSE114691 and GSE24129 from the GEO database were analyzed, revealing 5,788 differentially expressed genes (1,450 upregulated, 4,338 downregulated) between FGR and control placental samples. Functional enrichment analysis indicated that downregulated genes were primarily involved in mitochondrial function, aerobic respiration, and amino acid metabolism, while upregulated genes were associated with cell adhesion and histone modification. Weighted gene co-expression network analysis (WGCNA) identified 19 modules, with the darkorange module showing the strongest positive correlation with FGR. LASSO regression further selected eight candidate genes, among which only TRIP10 demonstrated consistent and significant upregulation in the independent validation dataset and exhibited excellent diagnostic performance (AUC = 0.906). Western blot confirmed significant upregulation of TRIP10 protein in FGR placental tissues. Functional assays in JEG-3 trophoblast cells revealed that TRIP10 knockdown significantly enhanced cell migration and invasion, while TRIP10 overexpression suppressed these processes. Collectively, this study identifies TRIP10 as a key gene significantly upregulated in FGR placentas and establishes TRIP10 as a negative regulator of trophoblast migration and invasion, suggesting that TRIP10 dysregulation may contribute to impaired placental development and FGR pathogenesis, representing a promising biomarker and potential therapeutic target.
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3. Maternal Metabolic Dysfunction and Uteroplacental Adaptation in Polyendocrine Metabolic Ovarian Syndrome Pregnancy.
PMID:日期:2026-10-01Polyendocrine metabolic ovarian syndrome (PMOS), formerly known as polycystic ovary syndrome (PCOS), is a multisystem endocrine-metabolic disorder that significantly increases the risk of adverse pregnancy outcomes, partly independently of obesity. PMOS patients frequently exhibit a characteristic metabolic-endocrine milieu of insulin resistance, hyperandrogenemia, dyslipidemia, and chronic low-grade inflammation. The physiological insulin resistance of pregnancy, driven by placental hormones, exacerbates these pre-existing disturbances and disrupts endometrial receptivity and placental function. These insults converge on conserved signaling pathways, phosphoinositide 3-kinase (PI3K)/ protein kinase B (AKT)/ mechanistic target of rapamycin (mTOR), nuclear factor kappa B (NF-κB)/ c-Jun N-terminal kinase (JNK), androgen receptor-mediated mitochondrial dysfunction and ferroptosis, and peroxisome proliferator-activated receptor (PPAR)-regulated lipid dysregulation, and impair trophoblast invasion, spiral artery remodeling, angiogenic balance, and nutrient transport. The resulting mitochondrial oxidative stress and lipotoxic injury contribute to early pregnancy loss, gestational diabetes, hypertensive disorders, preterm birth, and aberrant fetal growth. Concurrently, the dysmetabolic intrauterine environment programs offspring metabolic and reproductive dysfunction through epigenetic and developmental mechanisms. This review synthesizes current evidence linking the maternal metabolic milieu of PMOS to endometrial defects, placental structural and functional alterations, and long-term offspring outcomes. Emerging data on adipose-derived lipid mediators, fatty acid transporters, and inflammatory-metabolic crosstalk at the maternal-uteroplacental interface are examined. Therapeutic strategies such as lifestyle modification, metformin, and bariatric surgery in obese patients are appraised. Although some benefits have been reported, evidence across pregnancy outcomes remains inconsistent, and rigorous preconception trials are needed to establish efficacy. Elucidating how maternal metabolic signals contribute to placental injury and rigorously testing preconception interventions will be essential to refine risk stratification, develop targeted therapies, and interrupt the cycle of metabolic disease transmission in PMOS.
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6. Dysregulation of SCARB1 Alternative Splicing Disturbs Amino Acid Metabolism in Anembryonic Pregnancy.
PMID:日期:2026-09-23Anembryonic pregnancy (AP) accounts for a notable proportion of all first-trimester spontaneous miscarriage. Alternative splicing has been implicated in placental development and spontaneous abortion. However, the role of alternative splicing in modulating amino acid metabolism in AP remains unclear. We employed mass spectrometry to measure the levels of amino acids and metabolites in the serum of AP patients and healthy controls. RNA-Seq and rMATS were utilized to evaluate the alternative splicing profiles of chorionic villi from the two groups. Key splicing events in PRKCD, SCARB1, and METTL2B were subsequently validated by splicing-specific PCR. An integrated analysis, incorporating transcription factor prediction and publicly available datasets, was performed to explore the potential mechanisms by which alternative splicing may contribute to the metabolic disturbances in AP. Mass spectrometry analysis confirmed dysregulated of amino acid metabolism in AP. Compared to controls, AP patients exhibited 903 differentially alternative splicing genes and 558 differentially expressed genes, with skipping exons as the predominant alternative splicing type. Notably, PRKCD, SCARB1, and METTL2B displayed the most significant splicing changes, with preferential exon inclusion in AP samples. Motif analysis predicted that SCARB1 was a potential target gene of transcription factor TEAD4. Functional studies revealed that both SCARB1 and TEAD4 were involved in metabolism regulation, including amino acid and lipid metabolism. Our study demonstrates that dysregulation of alternative splicing in SCARB1 may contribute to AP by disrupting metabolic homeostasis, particularly amino acid metabolism. These findings highlight alternative splicing-mediated metabolic reprogramming as a potential mechanistic underpinning of AP.
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7. Beclin1 Regulates Sertoli Cell Function to Maintain Mouse Spermatogenesis.
PMID:日期:2026-09-23Besides providing nutrients, Sertoli cells support spermatogenic cells development by maintaining seminiferous epithelial polarity, forming the blood-testis barrier (BTB), and phagocytosing residual bodies. Beclin1, a core component of the autophagy initiation complex, is critical for autophagic flux in many cell types. However, its role in Sertoli cells remains unclear. Here, we generated a Sertoli cell-specific Becn1 knockout (cKO) mouse model and found that 9-week-old male cKO mice exhibited reduced fertility with decreased sperm quality and vacuolated seminiferous tubules, and became completely infertile by 12 weeks of age. These defects were associated with disrupted BTB integrity and reduced expression of Claudin-11 in the testes. Further analysis revealed that loss of Beclin1led to impaired autophagosome formation, evidenced by reduced LC3-II/LC3-I ratio. In summary, these findings demonstrate that Beclin1 in Sertoli cells is vital for spermatogenesis and male fertility.
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8. An Ex Vivo Model for the Onset of Human Labor.
PMID:日期:2026-09-23During gestation, the myometrium remains relaxed but undergoes a phenotypic transformation near term that initiates labor. This coincides with increased expression of contraction-associated proteins (CAPs) and decreased expression of relaxation-associated proteins (RAPs), thereby promoting the development of powerful synchronous contractions that deliver the fetus. We do not yet fully understand the biochemical signaling pathways and physiological changes that occur as human myometrium transitions from a non-laboring to a laboring phenotype. An ex vivo model for the onset of human labor can expand our knowledge. This study aimed to assess whether non-laboring pregnant human myometrium in culture undergoes a phenotypic transformation that is consistent with transitioning toward a labor-like phenotype. Term, non-laboring pregnant human myometrium biopsies were collected. A small portion was immediately snap-frozen (0 h time point), while the remaining tissue was dissected into small pieces, incubated for 48 h in serum-free medium, and then snap-frozen. Changes in the mRNA abundance of key myometrial genes were assessed by qRT-PCR, and protein levels were quantified by Western blotting. Data were analyzed using GraphPad Prism. Myometrial expression of key CAPs, including GJA1, ESR1, PTGS2, NFκB1, NFκB3, IL1β, IL6, and AKR1C1, increased significantly, while expression of the RAPs, PLCL1, HSPB1, and HSPB6, was decreased significantly after 48 h of ex vivo culture. Term, non-laboring pregnant human myometrial explants undergo coordinated molecular remodeling during 48 h of ex vivo culture, with many changes paralleling those reported at term labor in vivo. These findings support prolonged explant culture as a model of the molecular transition toward a labor-like state, while also demonstrating that cultured non-laboring explants may no longer faithfully represent the original non-laboring phenotype.
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9. MicroRNA-122-5p Targets FOXO3 to Mediate Podocyte Senescence and Proteinuria Induced by Angiotensin II Type 1 Receptor Autoantibodies in Preeclampsia.
PMID:日期:2026-09-22Preeclampsia (PE) drives irreversible podocyte depletion, predisposing patients to a heightened long-term risk of chronic kidney disease. While premature cellular senescence underlies this structural loss, the specific preeclamptic factors triggering this mechanism remain incompletely defined. We investigated the role of the angiotensin II type 1 receptor agonistic autoantibody (AT1-AA)-a central circulating pathogenic factor in PE-in promoting podocyte senescence through post-transcriptional pathways. We first interrogated public clinical transcriptomic datasets and validated the findings using clinical urine specimens from PE patients to identify key dysregulated microRNAs in PE. We then integrated in vitro mechanistic assays using human podocytes with an in vivo AT1-AA-infused pregnant mouse model. The regulatory cascade was validated via dual-luciferase reporter assays. The therapeutic efficacy of targeting this pathway was evaluated via systemic administration of a specific microRNA inhibitor (AntagomiR-122-5p). Bioinformatic analysis and clinical validation revealed that miR-122-5p is upregulated in PE patients. In vivo, AT1-AA exposure provoked classic PE manifestations, including severe hypertension, albuminuria, and podocyte foot process effacement. This pathology was driven by podocyte-specific senescence, evidenced by nuclear p21 accumulation and a senescence-associated secretory phenotype (SASP). Mechanistically, AT1-AA triggered a toxic accumulation of mitochondrial reactive oxygen species (mtROS) by upregulating miR-122-5p, which directly repressed the FOXO3/SOD2 antioxidant defense system. Targeted in vivo inhibition of miR-122-5p yielded dual therapeutic benefits: it attenuated the elevation in maternal systolic blood pressure and conferred direct cytoprotection to the glomerular filtration barrier. AntagomiR-122-5p effectively reversed glomerular senescence, suppressed local inflammatory cytokines, and restored podocyte ultrastructure. AT1-AA governs preeclamptic podocyte senescence and proteinuria by suppressing the FOXO3/SOD2 signaling axis via clinically relevant miR-122-5p. Systemic antagonism of miR-122-5p offers a comprehensive therapeutic strategy to simultaneously alleviate maternal hypertension and protect the renal filtration barrier from permanent structural decline.
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10. Taurine Attenuates Repeated Heat Stress-Induced Male Reproductive Dysfunction in Mice: Associations with HPG Axis Homeostasis and Hypothalamic Microglial Changes.
PMID:日期:2026-09-22Heat stress (HS)-induced male reproductive dysfunction is usually interpreted within a testis-centered framework, whereas the contribution of central neuroendocrine disturbance remains less well defined. In the present study, a repeated HS mouse model was used to examine whether taurine pretreatment attenuates reproductive dysfunction by integrating local testicular endpoints with HPG-axis-related and hypothalamic inflammatory readouts. Male C57BL/6J mice were assigned to control, HS + vehicle, and HS + taurine groups. Mice in the HS groups were exposed to 40 ± 1 °C for 1 h daily for 14 consecutive days, and taurine was administered intraperitoneally before each heat exposure. Sperm parameters, testicular histopathology, inflammatory, oxidative, apoptotic, endocrine, and hypothalamic microglial endpoints were assessed. Repeated HS impaired sperm motility and concentration, increased abnormal sperm morphology, and caused marked histopathological injury in the testes. These changes were accompanied by increased testicular inflammation, oxidative stress, and apoptosis. HS also disrupted HPG-axis hormone homeostasis, as reflected by altered hypothalamic Gnrh expression, pituitary Lhb and Fshb expression, and circulating reproductive hormone levels. In parallel, repeated HS was associated with hypothalamic microglial activation, increased inflammatory responses, and increased microglia-GnRH overlap. Taurine pretreatment significantly attenuated sperm dysfunction and testicular injury, reduced inflammatory, oxidative, and apoptotic alterations, partially restored endocrine homeostasis, and reduced hypothalamic microglial responses. Together, these findings show that taurine alleviates repeated HS-induced male reproductive dysfunction with coordinated improvements in testicular injury, endocrine imbalance, and hypothalamic inflammatory responses. However, the hypothalamic findings are associative and do not establish causality.