Background While maternal psychological stress during mid-to-late pregnancy has been linked to offspring allergies,the impact of early pregnancy distress remains unclear.This study investigates the association between...Background While maternal psychological stress during mid-to-late pregnancy has been linked to offspring allergies,the impact of early pregnancy distress remains unclear.This study investigates the association between maternal depressive and anxiety symptoms in early pregnancy and allergic diseases in offspring.Methods Based on a birth cohort of 5263 children,antenatal depressive and anxiety symptoms in early pregnancy were assessed via the Patient Health Questionnaire and Generalized Anxiety Disorder Questionnaire,respectively.Allergic outcomes,including asthma,atopic dermatitis(AD),and allergic rhinitis(AR),were evaluated via structured questionnaires.Relative risks(RRs)with 95%confidence intervals(CIs)were estimated via generalized linear models,whereas restricted cubic splines were used to explore linear and non-linear associations between maternal distress and allergic outcomes.Results Maternal depressive symptoms in early pregnancy were associated with an increased risk of AD[adjusted RR(95%CI)=1.15(1.03–1.29)]and AR[1.52(1.29–1.79)].Maternal anxiety symptoms in early pregnancy were associated with increased risks of AD[1.11(1.02–1.21),mild anxiety]and AR[1.33(1.04–1.68),moderate to severe anxiety].Dose‒response analyses revealed graded relationships between distress severity and allergic outcomes.In the joint analysis,comorbid depression and anxiety in early pregnancy were associated with an increased risk of AD[1.15(1.05–1.26)]and AR[1.42(1.23–1.63)].Subgroup analysis revealed a greater risk of asthma for boys born to mothers with mild anxiety[1.95(1.20–3.15)]but not for girls.Conclusion Maternal distress in early pregnancy is associated with an increased risk of allergic diseases in offspring during toddlerhood.展开更多
Huang et al.[1]have put forward reasonable suggestions regarding certain findings of our recently published article,specifically including:(i)the cut-off values and limitations of the Edinburgh Postnatal Depression Sc...Huang et al.[1]have put forward reasonable suggestions regarding certain findings of our recently published article,specifically including:(i)the cut-off values and limitations of the Edinburgh Postnatal Depression Scale(EPDS);(ii)the restriction of data collection in our study to the third trimester;(iii)the sampling methodology employed in this study;(iv)the use of binary versus ternary classification for EPDS scores;(v)the lack of 95%confidence intervals for prevalence estimates;and(vi)the assessment of participants’prior mental health history.As described in this Reply,we interpreted the results of our article by reviewing and referring to other published articles.展开更多
Antenatal depression is a significant contributor to maternal morbidity in the perinatal period[1].It has also been associated with an increased risk for premature delivery,decreased rates of breastfeeding initiation,...Antenatal depression is a significant contributor to maternal morbidity in the perinatal period[1].It has also been associated with an increased risk for premature delivery,decreased rates of breastfeeding initiation,and a broad range of adverse child out-comes,including emotional problems,externalizing difficulties,attachment issues,and poorer cognitive development[2-6]Depression in the antenatal period may persist postnatally and increase in severity further exacerbating the negative conse-quences.There are considerable geographical differences in ante-natal depression prevalence rates across China,ranging from 9.8%to 35.4%,which is likely due to variations in demographic,lifestyle,social,and economic factors[7,8].Heterogeneity in study design and data source has also resulted in these wide variations.Further,previous Chinese studies examining antenatal depression have been limited due to relatively small sample sizes,short study peri-ods,and a focus on only one specific geographical district.Limited prevalence data in China suggest that a large-scale multi-center study is warranted.展开更多
Sperm motility and morphology are indispensable for sperm-egg interaction and successful fertilization.However,the RNA splicing mechanisms in an m6A-dependent manner regulating spermiogenesis-related genes remain poor...Sperm motility and morphology are indispensable for sperm-egg interaction and successful fertilization.However,the RNA splicing mechanisms in an m6A-dependent manner regulating spermiogenesis-related genes remain poorly defined,and targeted therapy strategies to restore impaired sperm motility and morphology are lacking.In this study,we identify heterogeneous nuclear ribonucleoprotein R(hnRNPR)as a critical m6A-dependent splicing mediator.Pathogenic mutations in HNRNPR cause sperm motility decline,morphological abnormality,and male infertility in both humans and mice.Mechanistically,Hnrnpr mutation disrupts m6A-dependent splicing of Skap2 pre-mRNA,thus impairing cytoskeletal structure and mitochondrial organization in sperm.Consistently,specific knockout of Skap2 in male germ cells displays sperm abnormalities,which phenocopy those observed in humans and mice with Hnrnpr mutants,unveiling a functional hnRNPR-SKAP2 axis.Leveraging these insights,we developed a therapeutic strategy to restore sperm motility and morphology,relying on extracellular vesicle-mediated SKAP2 delivery to enter the efferent ductules of the testicles,which could promote sperm cytoskeletal remodeling and mitochondrial organization.Notably,the co-culture of extracellular vesicle SKAP2 with human and mouse sperms also significantly enhanced the sperm motility.Altogether,these findings identify hnRNPR as a pivotal regulator of m6A-mediated Skap2 splicing during spermiogenesis and highlight extracellular vesicle SKAP2 as a promising therapeutic target for poor sperm quality and male infertility.展开更多
Background and Objectives:Previous studies have reported there were associations between ovarian function and dietary factors,metabolic factors and gut microbiota.However,it is unclear whether causal associations exis...Background and Objectives:Previous studies have reported there were associations between ovarian function and dietary factors,metabolic factors and gut microbiota.However,it is unclear whether causal associations exist.We aimed to explore the causal relationship of these factors with risk of primary ovarian failure(POF).Methods and Study Design:Two-sample Mendelian randomization(MR)analysis was performed to genetically predict the causal effects of dietary and metabolic factors and gut microbiota on POF.The inverse variance weighted(IVW)method was used as the primary statistical method.A series of sensitivity analyses,including weighted median,MR-Egger,simple mode,weighted mode methods,and leave-one-out analysis,were conducted to assess the robustness of the MR analysis results.Results:IVW analysis revealed that cigarettes smoked per day,coffee intake and cooked vegetable intake were not causally correlated with POF at the genetic level.However,POF were associated with fresh fruit intake,BMI,Eubacterium(hallii group),Eubacterium(ventriosum group),Ad lercreutzia,Intestinibacter,Lachnospiraceae(UCG008),and Terrisporobacter.These findings were robust ac cording to extensive sensitivity analyses.Conclusions:This study identified several dietary factors,metabolic factors and gut microbiota taxa that may be causally implicated in POF,potentially offering new therapeutic tar gets.展开更多
Objective:Frozen-thawed embryo transfer(FET)is widely used inin vitro fertilization(IVF)clinics but is associated with an increased risk of several pregnancy complications,including large-for-gestational age and place...Objective:Frozen-thawed embryo transfer(FET)is widely used inin vitro fertilization(IVF)clinics but is associated with an increased risk of several pregnancy complications,including large-for-gestational age and placenta-related diseases.However,the effects of FET on placentation remain unclear.Therefore,we used single-cell RNA-sequencing(scRNA-seq)technology to investigate the impact of FET on placental gene expression in different subtypes of trophoblasts.Methods:A mouse model of IVF and FET was constructed to collect placenta tissues.scRNA-seq was performed on placentas from two dams undergoing IVF-embryo transfer and two dams undergoing IVF-FET.Differentially expressed gene(DEG)analyses were performed in different subtypes of trophoblasts.Identified DEGs were polymerase chain reaction(PCR)validated.Results:The fetal weights and placental efficiency were higher in the FET group than those in the IVF group at E18.5,with no significant difference in placental weights.Subsequently,55,406 placental cells were captured and annotated.Upregulated DEGs in the FET group in syncytiotrophoblasts(SynTs)and sinusoidal trophoblast giant cells(S-TGCs)within the placental labyrinth were enriched in pathways related to vascular development and oxidative stress,respectively.The expression of the imprinted geneIgf2 in SynTs,S-TGCs,and spongiotrophoblasts was significantly increased.In the junctional zone,FET upregulated the expression of prolactin genes such asPrl3b1 in glycogen trophoblasts(GlyTs)while the downregulated expression of GlyT genes following FET was associated with mesenchyme development.Conclusions:This study first identifies DEGs and enriched pathways in different subtypes of trophoblasts following FET.These genes and pathways may contribute to the increased placental efficiency and fetal weights.Future studies are required to confirm these results and further explore the key mechanisms in placental pathologies.展开更多
Polycystic ovary syndrome(PCOS)is a frequent endocrine and metabolic imbalance that typically occurs in women of reproductive age.Its molecular pathophysiology is yet unknown,especially the ovarian cellular metabolic ...Polycystic ovary syndrome(PCOS)is a frequent endocrine and metabolic imbalance that typically occurs in women of reproductive age.Its molecular pathophysiology is yet unknown,especially the ovarian cellular metabolic inefficiency that causes the transcriptional dysregulation of key genes linked to PCOS.Here,we discovered that one transcriptional-like regulator that causes PCOS is nuclear pyruvate kinase M2(nPKM2).Using multiomics techniques,we show that enhanced lactylation of histone 3 on lysine residues 9 and 18 is linked to nPKM2 binding to the genome,changing the three-dimensional architecture of the genome.Genomic compartment switching,topologically associated domain fusion,and novel enhancer–promoter interactions subsequently enhance the expression of PCOS-related genes,including CYP17A1 and CYP11A1.In mice,ectopic expression of Pkm2 in female GCs consistently presented PCOS-like traits,such as interrupted estrous cycles,hyperandrogenism,and so on.Importantly,whole-organ tracing imaging directly unfolded the number of small follicles,which increased highly in Pkm2-tdtomato transgene mice compared with control.Furthermore,pharmacological inhibition of the nuclear accumulation of PKM2 mitigated PCOS-like symptoms in mice and restored a wild-type-like transcriptome.This study demonstrates the important function of PKM2-mediated histone lactylation in regulating the three-dimensional chromatin architecture and highlights PKM2 as a potential therapeutic target for PCOS treatment.展开更多
Sperm quality refers to the functional characteristics of spermatozoa,encompassing their concentration,morphological normality,and progressive motility,which collectively determine their potential to achieve fertiliza...Sperm quality refers to the functional characteristics of spermatozoa,encompassing their concentration,morphological normality,and progressive motility,which collectively determine their potential to achieve fertilization.Declines in sperm quality are generally termed as oligozoospermia,teratozoospermia,or asthenozoospermia.展开更多
基金supported by National Key Research and Development Program of China(2022YFC2703500)National Natural Science Foundation of China(8211101588,82088102 and 82171686)+10 种基金Program of Shanghai Academic Research Leader(20XD1424100)Natural Science Foundation of Shanghai(20ZR1463100)Clinical research program of Shanghai Municipal Health Commission(202340222)Collaborative Innovation Program of Shanghai Municipal Health Commission(2020CXJQ01)Clinical Research Plan of Shanghai Shenkang Hospital Development Center(SHDC2023CRD001 and SHDC2020CR1008A)STI2030-Major Projects(2021ZD0200700)CAMS Innovation Fund for Medical Sciences(2019-I2M-5–064)Shanghai Clinical Research Center for Gynecological Diseases(22MC1940200)Shanghai Urogenital System Diseases Research Center(2022ZZ01012)Key Discipline Construction Project(2023–2025)of Three-Year Initiative Plan for Strengthening Public Health System Construction in Shanghai(GWVI-11.1–35)the specific research fund of the Innovation Platform for Academicians of Hainan Province(YSPTZX202311)and Shanghai Frontiers Science Research Base of Reproduction and Development.
文摘Background While maternal psychological stress during mid-to-late pregnancy has been linked to offspring allergies,the impact of early pregnancy distress remains unclear.This study investigates the association between maternal depressive and anxiety symptoms in early pregnancy and allergic diseases in offspring.Methods Based on a birth cohort of 5263 children,antenatal depressive and anxiety symptoms in early pregnancy were assessed via the Patient Health Questionnaire and Generalized Anxiety Disorder Questionnaire,respectively.Allergic outcomes,including asthma,atopic dermatitis(AD),and allergic rhinitis(AR),were evaluated via structured questionnaires.Relative risks(RRs)with 95%confidence intervals(CIs)were estimated via generalized linear models,whereas restricted cubic splines were used to explore linear and non-linear associations between maternal distress and allergic outcomes.Results Maternal depressive symptoms in early pregnancy were associated with an increased risk of AD[adjusted RR(95%CI)=1.15(1.03–1.29)]and AR[1.52(1.29–1.79)].Maternal anxiety symptoms in early pregnancy were associated with increased risks of AD[1.11(1.02–1.21),mild anxiety]and AR[1.33(1.04–1.68),moderate to severe anxiety].Dose‒response analyses revealed graded relationships between distress severity and allergic outcomes.In the joint analysis,comorbid depression and anxiety in early pregnancy were associated with an increased risk of AD[1.15(1.05–1.26)]and AR[1.42(1.23–1.63)].Subgroup analysis revealed a greater risk of asthma for boys born to mothers with mild anxiety[1.95(1.20–3.15)]but not for girls.Conclusion Maternal distress in early pregnancy is associated with an increased risk of allergic diseases in offspring during toddlerhood.
文摘Huang et al.[1]have put forward reasonable suggestions regarding certain findings of our recently published article,specifically including:(i)the cut-off values and limitations of the Edinburgh Postnatal Depression Scale(EPDS);(ii)the restriction of data collection in our study to the third trimester;(iii)the sampling methodology employed in this study;(iv)the use of binary versus ternary classification for EPDS scores;(v)the lack of 95%confidence intervals for prevalence estimates;and(vi)the assessment of participants’prior mental health history.As described in this Reply,we interpreted the results of our article by reviewing and referring to other published articles.
基金supported by the STI2030-Major Projects(2021ZD0200700)the National Key Research and Development Program of China(2021YFC2701600 and 2022YFC2703500)+10 种基金the National Natural Science Foundation of China(82088102 and 82301719)Science and Technology Innovation Fund of Shanghai Jiao Tong University(YG2020YQ29)Collaborative Innovation Program of Shanghai Municipal Health Commission(2020CXJQ01)Shanghai Municipal Commission of Health(20224Y0085 and 202340222)Open Fund Project of Guangdong Academy of Medical Sciences(YKY-KF202202)CAMS Innovation Fund for Medical Sciences(2019-I2M-5-064)Shanghai Clinical Research Center for Gynecological Diseases(22MC1940200)Shanghai Urogenital Sys-tem Diseases Research Center(2022ZZ01012)Key Discipline Con-struction Project(2023-2025)of Three-Year Initiative Plan for Strengthening Public Health System Construction in Shanghai(GWVI-11.1-35 and GWVI-11.2-YQ29)Shanghai Sailing Program(22YF1453100)Shanghai Frontiers Science Research Base of Reproduction and Development.
文摘Antenatal depression is a significant contributor to maternal morbidity in the perinatal period[1].It has also been associated with an increased risk for premature delivery,decreased rates of breastfeeding initiation,and a broad range of adverse child out-comes,including emotional problems,externalizing difficulties,attachment issues,and poorer cognitive development[2-6]Depression in the antenatal period may persist postnatally and increase in severity further exacerbating the negative conse-quences.There are considerable geographical differences in ante-natal depression prevalence rates across China,ranging from 9.8%to 35.4%,which is likely due to variations in demographic,lifestyle,social,and economic factors[7,8].Heterogeneity in study design and data source has also resulted in these wide variations.Further,previous Chinese studies examining antenatal depression have been limited due to relatively small sample sizes,short study peri-ods,and a focus on only one specific geographical district.Limited prevalence data in China suggest that a large-scale multi-center study is warranted.
基金supported by the National Natural Science Foundation of China(82088102)CAMS Innovation Fund for Medical Sciences(2019-I2M-5-064)+5 种基金Collaborative Innovation Program of Shanghai Municipal Health Commission(2020CXJQ01)Key Discipline Construction Project(2023-2025)of Three-Year Initiative Plan for Strengthening Public Health System Construction in Shanghai(GWVI-11.1-35)Shanghai Clinical Research Center for Gynecological Diseases(22MC1940200)Shanghai Urogenital System Diseases Research Center(2022ZZ01012)Shanghai Frontiers Science Research Center of Reproduction and Development,the Shenzhen portion of the Hetao Shenzhen-Hong Kong Science and Technology Innovation Cooperation Zone(program grant#HZQSWS-KCCYB2024031)China Postdoctoral Science Foundation under Grant Number 2025M782263。
文摘Sperm motility and morphology are indispensable for sperm-egg interaction and successful fertilization.However,the RNA splicing mechanisms in an m6A-dependent manner regulating spermiogenesis-related genes remain poorly defined,and targeted therapy strategies to restore impaired sperm motility and morphology are lacking.In this study,we identify heterogeneous nuclear ribonucleoprotein R(hnRNPR)as a critical m6A-dependent splicing mediator.Pathogenic mutations in HNRNPR cause sperm motility decline,morphological abnormality,and male infertility in both humans and mice.Mechanistically,Hnrnpr mutation disrupts m6A-dependent splicing of Skap2 pre-mRNA,thus impairing cytoskeletal structure and mitochondrial organization in sperm.Consistently,specific knockout of Skap2 in male germ cells displays sperm abnormalities,which phenocopy those observed in humans and mice with Hnrnpr mutants,unveiling a functional hnRNPR-SKAP2 axis.Leveraging these insights,we developed a therapeutic strategy to restore sperm motility and morphology,relying on extracellular vesicle-mediated SKAP2 delivery to enter the efferent ductules of the testicles,which could promote sperm cytoskeletal remodeling and mitochondrial organization.Notably,the co-culture of extracellular vesicle SKAP2 with human and mouse sperms also significantly enhanced the sperm motility.Altogether,these findings identify hnRNPR as a pivotal regulator of m6A-mediated Skap2 splicing during spermiogenesis and highlight extracellular vesicle SKAP2 as a promising therapeutic target for poor sperm quality and male infertility.
基金funded by National Key Research and De velopment Program of China(No.2022YFC2703803,No.2022YFC2703001,No.2021YFC2700603)National Natural Science Foundation of China(No.82088102,No.82171613,No.82171688)+5 种基金CAMS Innovation Fund for Medical Sciences(2019-I2M-5-064)Collaborative Innovation Program of Shanghai Municipal Health Commission(2020CXJQ01)Key Discipline Construction Project(2023-2025)of Three-Year Initiative Plan for Strengthening Public Health System Con struction in Shanghai(GWVI-11.1-35)Shanghai Clinical Re search Center for Gynecological Diseases(22MC1940200)Shanghai Urogenital System Diseases Research Center(2022ZZ01012)Shanghai Frontiers Science Research Center of Reproduction and Development,Zhejiang Province College Student Science and Technology Innovation Program(Xinmiao Plan)(2023R401210).
文摘Background and Objectives:Previous studies have reported there were associations between ovarian function and dietary factors,metabolic factors and gut microbiota.However,it is unclear whether causal associations exist.We aimed to explore the causal relationship of these factors with risk of primary ovarian failure(POF).Methods and Study Design:Two-sample Mendelian randomization(MR)analysis was performed to genetically predict the causal effects of dietary and metabolic factors and gut microbiota on POF.The inverse variance weighted(IVW)method was used as the primary statistical method.A series of sensitivity analyses,including weighted median,MR-Egger,simple mode,weighted mode methods,and leave-one-out analysis,were conducted to assess the robustness of the MR analysis results.Results:IVW analysis revealed that cigarettes smoked per day,coffee intake and cooked vegetable intake were not causally correlated with POF at the genetic level.However,POF were associated with fresh fruit intake,BMI,Eubacterium(hallii group),Eubacterium(ventriosum group),Ad lercreutzia,Intestinibacter,Lachnospiraceae(UCG008),and Terrisporobacter.These findings were robust ac cording to extensive sensitivity analyses.Conclusions:This study identified several dietary factors,metabolic factors and gut microbiota taxa that may be causally implicated in POF,potentially offering new therapeutic tar gets.
基金National Key Research and Development Program of China(2021YFC2700700,2022YFC2703500)National Natural Science Foundation of China(82171686)+4 种基金Clinical Research Program of Shanghai Municipal Health Commission(202340222)Natural Science Foundation of Shanghai(20ZR1463100)Clinical Research Plan of Shanghai Shenkang Hospital Development Center(SHDC2023CRD001)Shanghai Clinical Research Center for Gynecological Diseases(22MC1940200)Shanghai Urogenital System Diseases Research Center(2022ZZ01012)。
文摘Objective:Frozen-thawed embryo transfer(FET)is widely used inin vitro fertilization(IVF)clinics but is associated with an increased risk of several pregnancy complications,including large-for-gestational age and placenta-related diseases.However,the effects of FET on placentation remain unclear.Therefore,we used single-cell RNA-sequencing(scRNA-seq)technology to investigate the impact of FET on placental gene expression in different subtypes of trophoblasts.Methods:A mouse model of IVF and FET was constructed to collect placenta tissues.scRNA-seq was performed on placentas from two dams undergoing IVF-embryo transfer and two dams undergoing IVF-FET.Differentially expressed gene(DEG)analyses were performed in different subtypes of trophoblasts.Identified DEGs were polymerase chain reaction(PCR)validated.Results:The fetal weights and placental efficiency were higher in the FET group than those in the IVF group at E18.5,with no significant difference in placental weights.Subsequently,55,406 placental cells were captured and annotated.Upregulated DEGs in the FET group in syncytiotrophoblasts(SynTs)and sinusoidal trophoblast giant cells(S-TGCs)within the placental labyrinth were enriched in pathways related to vascular development and oxidative stress,respectively.The expression of the imprinted geneIgf2 in SynTs,S-TGCs,and spongiotrophoblasts was significantly increased.In the junctional zone,FET upregulated the expression of prolactin genes such asPrl3b1 in glycogen trophoblasts(GlyTs)while the downregulated expression of GlyT genes following FET was associated with mesenchyme development.Conclusions:This study first identifies DEGs and enriched pathways in different subtypes of trophoblasts following FET.These genes and pathways may contribute to the increased placental efficiency and fetal weights.Future studies are required to confirm these results and further explore the key mechanisms in placental pathologies.
基金supported by the Medical Science Data Center of Fudan University and the Big Data Computing Center of Southeast University.We thank the National Natural Science Foundation of China(82088102,82271669,and 81671412)the National Key Research and Development Program of China(2022YFC2703600)+7 种基金the International Cooperation Project of China and Canada NSFC(81661128010)the Collaborative Innovation Program of Shanghai Municipal Health Commission(2020CXJQ01)the Key Discipline Construction Project(2023-2025)of the Three-Year Initiative Plan for Strengthening Public Health System Construction in Shanghai(GWVI-11.1-35)the Clinical Research Plan of SHDC(SHDC2020CR1008A)the Shanghai Clinical Research Center for Gynecological Diseases(22MC1940200)the Shanghai Urogenital System Diseases Research Center(2022ZZ01012)the CAMS Innovation Fund for Medical Sciences(2019-I2M-5-064)the Shanghai Frontiers Science Research Center of Reproduction and Development.Postdoctoral grant(2018M630454)。
文摘Polycystic ovary syndrome(PCOS)is a frequent endocrine and metabolic imbalance that typically occurs in women of reproductive age.Its molecular pathophysiology is yet unknown,especially the ovarian cellular metabolic inefficiency that causes the transcriptional dysregulation of key genes linked to PCOS.Here,we discovered that one transcriptional-like regulator that causes PCOS is nuclear pyruvate kinase M2(nPKM2).Using multiomics techniques,we show that enhanced lactylation of histone 3 on lysine residues 9 and 18 is linked to nPKM2 binding to the genome,changing the three-dimensional architecture of the genome.Genomic compartment switching,topologically associated domain fusion,and novel enhancer–promoter interactions subsequently enhance the expression of PCOS-related genes,including CYP17A1 and CYP11A1.In mice,ectopic expression of Pkm2 in female GCs consistently presented PCOS-like traits,such as interrupted estrous cycles,hyperandrogenism,and so on.Importantly,whole-organ tracing imaging directly unfolded the number of small follicles,which increased highly in Pkm2-tdtomato transgene mice compared with control.Furthermore,pharmacological inhibition of the nuclear accumulation of PKM2 mitigated PCOS-like symptoms in mice and restored a wild-type-like transcriptome.This study demonstrates the important function of PKM2-mediated histone lactylation in regulating the three-dimensional chromatin architecture and highlights PKM2 as a potential therapeutic target for PCOS treatment.
基金supported by grants from Shenzhen portion of the Hetao Shenzhen-Hong Kong Science and Technology Innovation Cooperation Zone(HZQSWS-KCCYB-2024031)the National Key R&D Program of China(2022YFC2702902)+4 种基金the Medical New Technology Research and Transformation Seed Plan of Shanghai Municipal Health Commission(2024ZZ2018)the Clinical Research Project of the Shanghai Municipal Commission of Shanghai Municipal Health Commission(20224Y0085)the Youth Project of the National Natural Science Foundation of China(82003489)the National Natural Science Foundation of China(82273663,32370574)the Open Fund of the Key Laboratory of Reproductive Genetics(Zhejiang University),Ministry of Education(ZDFY2024-RG-2).
文摘Sperm quality refers to the functional characteristics of spermatozoa,encompassing their concentration,morphological normality,and progressive motility,which collectively determine their potential to achieve fertilization.Declines in sperm quality are generally termed as oligozoospermia,teratozoospermia,or asthenozoospermia.
