Molecular genetics and metabolism最新文献

{"title":"Should the “mitochondrial cocktail” be a default option? An opinion","authors":"Peter W. Stacpoole , Stephen D. Cederbaum","doi":"10.1016/j.ymgme.2025.109264","DOIUrl":"10.1016/j.ymgme.2025.109264","url":null,"abstract":"","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 4","pages":"Article 109264"},"PeriodicalIF":3.5,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145371161","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Letter to the editors: Supervised machine learning prediction of genotype–phenotype correlations in PMM2-CDG, in response to Pajusalu et al. [3]","authors":"Julia Boonnak","doi":"10.1016/j.ymgme.2025.109256","DOIUrl":"10.1016/j.ymgme.2025.109256","url":null,"abstract":"","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 3","pages":"Article 109256"},"PeriodicalIF":3.5,"publicationDate":"2025-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Urinary tetraglucoside excretion as a biomarker in liver glycogen storage diseases","authors":"Ruben J. Overduin ,&nbsp;Candelas Gross-Valle ,&nbsp;Joost Groen ,&nbsp;Jennifer van der Krogt ,&nbsp;Christa A. Koops ,&nbsp;Terry G.J. Derks ,&nbsp;M. Rebecca Heiner-Fokkema ,&nbsp;Andrea B. Haijer-Schreuder","doi":"10.1016/j.ymgme.2025.109263","DOIUrl":"10.1016/j.ymgme.2025.109263","url":null,"abstract":"<div><h3>Introduction</h3><div>Increased urinary tetraglucoside (Glc4) excretions are associated with abnormal glycogen metabolism. While Glc4 is an established biomarker for glycogen storage disease (GSD) type II, a traditional <em>muscle</em> GSD, little data is available on excretions in <em>liver</em> GSD.</div></div><div><h3>Methods</h3><div>A single-center retrospective analysis was conducted on urinary Glc4 samples obtained during routine clinical care of 99 individuals with liver GSD, including 9 patients with Glc4 samples taken as part of the diagnostic work-up (i.e., before treatment) and 5 patients with Glc4 samples after liver transplantation.</div></div><div><h3>Results</h3><div>Glc4 excretions were increased at time of diagnosis in 1/1 GSD IIIa, 3/3 GSD IXa, 1/2 GSD IXa female carrier, 0/1 GSD IXb and 2/2 Fanconi-Bickel syndrome patients. In 8/9 of these patients with samples in the diagnostic work-up, subsequent follow-up samples were available, displaying that Glc4 excretions decreased after initiation of GSD management in 8/8 patients, and in 6/8 patients Glc4 excretions were within the reference range on last follow-up. Analysis of Glc4 samples in the monitoring phase revealed that, despite management, Glc4 excretions were elevated in the majority of GSD Ia (17/27) and Ib (6/10), and <em>all</em> GSD IIIa (19/19), GSD IIIb (4/4), and IXc (1/1) patients. In contrast, increased Glc4 excretions were less frequently observed in GSD IV (1/6), GSD VI (1/2), IXa (4/19), IXa female carrier (0/1), IXb (0/2), and Fanconi-Bickel syndrome (2/4) patients during clinical follow-up. After liver transplantation in a GSD Ia and a GSD Ib patient, Glc4 excretions normalized.</div></div><div><h3>Conclusion</h3><div>Urinary Glc4 may be a useful additional biomarker in liver GSD patients, both in the diagnostic work-up and in the monitoring phase. Future studies could additionally assess the role of Glc4 as response biomarker in drug development.</div><div>Take-home message: Urinary Glc4 may be a useful additional biomarker in liver GSD patients, both in the diagnostic work-up and in the monitoring phase.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 3","pages":"Article 109263"},"PeriodicalIF":3.5,"publicationDate":"2025-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effectiveness of newborn screening for X-linked disorders in females: A scoping review","authors":"Hanabi Geiger,&nbsp;Yutaka Furuta,&nbsp;John A. Phillips III,&nbsp;Rory J. Tinker","doi":"10.1016/j.ymgme.2025.109262","DOIUrl":"10.1016/j.ymgme.2025.109262","url":null,"abstract":"<div><h3>Purpose</h3><div>Newborn screening (NBS) identifies thousands of infants annually with conditions amenable to early intervention. Although several X-linked (XL) conditions in NBS panels are viewed as primarily male disorders, emerging evidence shows females also present clinically. This scoping review evaluates NBS efficacy for detecting XL conditions in females.</div></div><div><h3>Methods</h3><div>Twelve XL genetic disorders were identified through cross-referencing the Recommended Uniform Screening Panel, American College of Medical Genetics ACT sheets, and available literature. A systematic search and scoping review identified studies reporting NBS outcomes.</div></div><div><h3>Results</h3><div>All twelve XL disorders reviewed affect females, often with milder phenotypes, likely due to X-inactivation. However, only 6/12 (50 %) of these conditions had relevant NBS data, and female cases were rare. Only 92/221 (42 %) of the studies included detected female cases. Skewed X-inactivation may modulate expression, leading to biomarker levels within reference ranges and reducing detection.</div></div><div><h3>Conclusions</h3><div>Although XL conditions affect both sexes, current NBS protocols rarely detect females or don't report sex-specific data at all. This absence highlights broader gaps in how screening outcomes are reported. Addressing these limitations may require sex-specific biomarker thresholds, alternative biomarkers, or genetic testing. Such efforts are necessary to ensure that NBS programs equitably serve all affected newborns.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 3","pages":"Article 109262"},"PeriodicalIF":3.5,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Novel murine model provides insights into early-onset of kidney disease in glycogen storage disease type Ib","authors":"Kunal Pratap,&nbsp;Cheol Lee,&nbsp;Lisa Zhang,&nbsp;Hung Dar Chen,&nbsp;Irina Arnaoutova,&nbsp;Brian C. Mansfield,&nbsp;Janice Y. Chou","doi":"10.1016/j.ymgme.2025.109258","DOIUrl":"10.1016/j.ymgme.2025.109258","url":null,"abstract":"<div><div>Glycogen storage disease type Ib (GSD-Ib), caused by a deficiency of the glucose-6-phosphate transporter (G6PT), is characterized by impaired glucose homeostasis and progressive renal dysfunction. Using <em>G6pt</em>-deficient (<em>G6pt</em>−/−) mice, which closely recapitulate the pathophysiology of GSD-Ib, we previously demonstrated that GSD-Ib nephropathy is marked by disrupted renal homeostasis, acute kidney injury, and fibrosis. However, due to the severity of the metabolic defect, <em>G6pt</em>−/− mice typically fail to survive beyond three weeks of age, limiting the study of disease progression in adulthood. To overcome this limitation, we generated liver human G6PT-augmented, kidney G6PT-deficient (L-hG6PT/K^−/−) mice, which restore hepatic G6PT expression to support survival while maintaining G6PT deficiency in the kidney. We show that adult L-hG6PT/K^−/− mice develop renal abnormalities similar to those seen in 3-week-old global <em>G6pt</em>−/− mice. Importantly, unlike the younger cohort, 12-week-old L-hG6PT/K^−/− mice exhibit a progressive decline in renal function accompanied by marked fibrosis. These findings establish L-hG6PT/K^−/− mice as a robust and physiologically relevant model for investigating the mechanisms and progression of GSD-Ib nephropathy in mature animals.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 3","pages":"Article 109258"},"PeriodicalIF":3.5,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adenylosuccinate synthetase deficiency and purine nucleotide cycle disruption impair neuromuscular function in Caenorhabditis elegans","authors":"Rishika R. Patil,&nbsp;Latisha P. Franklin,&nbsp;Melinda D. Jin,&nbsp;Wendy Hanna-Rose","doi":"10.1016/j.ymgme.2025.109261","DOIUrl":"10.1016/j.ymgme.2025.109261","url":null,"abstract":"<div><div>The critical role of the purine nucleotide cycle (PNC) in human health is underscored by the fact that mutations in adenylosuccinate synthetase (ADSS) and adenylosuccinate lyase (ADSL), two of its three enzymes, are associated with severe inborn errors of purine metabolism. We use <em>Caenorhabditis elegans</em> to investigate the biological roles of the PNC and to characterize developmental and behavioral functions of ADSS and ADSL. Here we report that <em>adss-1</em>, which encodes ADSS in <em>C. elegans</em>, is required for fertility and locomotion. <em>adss-1</em> loss-of-function mutants also have small body size, and their development is severely delayed. These phenotypes are shared with <em>adsl-1</em>, which encodes ADSL, suggesting that an intact PNC is required for <em>C. elegans</em> development. Interestingly, <em>adss-1</em> and <em>adsl-1</em> each have unique phenotypes not shared with the other. <em>adss-1</em>-specific phenotypes include excessive excitatory (or decreased inhibitory) synaptic transmission at the neuromuscular junction and impaired mechanosensation, suggesting an important function in the nervous system. We have also established a powerful model for further investigation of how ADSS activity impacts mobility, providing insight into the poorly understood molecular mechanisms driving phenotypic outcomes in ADSS1 deficiency.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 3","pages":"Article 109261"},"PeriodicalIF":3.5,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308528","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Detecting mitochondrial electron transport chain enzyme defects in low-heteroplasmy single large-scale mtDNA deletion syndromes (SLSMDSs)","authors":"Xueyang Pan ,&nbsp;Yue Wang ,&nbsp;Ning Liu ,&nbsp;Xi Luo ,&nbsp;V. Reid Sutton ,&nbsp;William J. Craigen ,&nbsp;Qin Sun","doi":"10.1016/j.ymgme.2025.109260","DOIUrl":"10.1016/j.ymgme.2025.109260","url":null,"abstract":"<div><div>Large deletions in multi-copy mitochondrial DNA (mtDNA) are associated with chronic progressive external ophthalmoplegia (CPEO), Kearns-Sayre syndrome (KSS), and Pearson syndrome (PS), collectively referred to as single large-scale mtDNA deletion syndromes (SLSMDSs). These deletions are typically sporadic and heteroplasmic, yet the relationship between heteroplasmy levels and disease severity remains uncertain, particularly for low level deletions, making pathogenicity assessment challenging.</div><div>To evaluate the functional impact of mtDNA deletions in muscle, we retrospectively analyzed 1104 consecutive clinical cases with both mtDNA sequencing and mitochondrial electron transport chain (ETC) enzyme assays performed on the same muscle specimen. Fifteen cases (1.4 %) carried a single large mtDNA deletion and exhibited clinical features consistent with the CPEO/KSS spectrum. Of these, seven showed ETC deficiencies despite low deletion heteroplasmy levels (&lt;10 % in all cases). Four had enzyme deficiencies defined to a single complex, while three had deficiencies in multiple complexes. Complex IV was most frequently impaired, whereas nuclear-encoded complex II activity remained normal in all samples. Notably, the pattern of ETC impairment did not fully correlate with the specific mitochondrial genes disrupted by the deletions.</div><div>These findings demonstrate that mitochondrial dysfunction can occur at mtDNA deletion heteroplasmy levels far below conventional pathogenic thresholds. This highlights the diagnostic relevance of low-level mtDNA deletions and supports the integration of molecular and functional testing in accurate SLSMDS diagnosis.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 3","pages":"Article 109260"},"PeriodicalIF":3.5,"publicationDate":"2025-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145292996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mucopolysaccharidosis VI: Therapeutic strategies and perspectives","authors":"Andrés Felipe Leal ,&nbsp;Luis Eduardo Prieto ,&nbsp;Harry Pachajoa ,&nbsp;Shunji Tomatsu","doi":"10.1016/j.ymgme.2025.109255","DOIUrl":"10.1016/j.ymgme.2025.109255","url":null,"abstract":"<div><div>Mucopolysaccharidosis VI, also known as Maroteaux-Lamy syndrome, is a lysosomal storage disorder (LSD) caused by pathogenic mutations in the <em>ARSB</em> gene, resulting in arylsulfatase (ARSB) deficiency and the lysosomal accumulation of dermatan sulfate (DS) and chondroitin 4-sulfate (C4S). DS and C4S accumulation leads to multisystemic symptoms in MPS VI patients in cartilage, bone, heart valves, cornea, liver, and respiratory tract. Currently, enzyme replacement therapy (ERT) is the only approved treatment for patients with MPS VI, providing clinical benefits that include increased survival and improved quality of life. However, ERT has a limited impact on bone manifestations. Significant advances have been made in gene therapy (GT) using classical adeno-associated virus and the CRISPR/Cas9 system, providing promising alternatives in MPS VI. Importantly, hematopoietic stem cell transplantation (HSCT) in combination with GT may also offer a novel alternative. Additionally, substrate reduction therapy with odiparcil, immunomodulation, and stop codon read-through therapies have been explored in MPS VI. Future directions in MPS VI should include targeting cellular alterations, such as mitochondrial dysfunction, exploring cartilage-targeting alternatives, and implementing pharmacological chaperones. This manuscript highlights recent progress and emerging strategies for treating MPS VI.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 3","pages":"Article 109255"},"PeriodicalIF":3.5,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145258515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amino acid supplementation in patients affected by leukoencephalopathies associated with mitochondrial aminoacyl tRNA synthetase pathogenic variants: Pilot clinical trial in adults and review of literature","authors":"Alessia Catania ,&nbsp;Silvia Marchet ,&nbsp;Krisztina Einvag ,&nbsp;Eleonora Lamantea ,&nbsp;Ettore Salsano ,&nbsp;Daniele Ghezzi ,&nbsp;Costanza Lamperti","doi":"10.1016/j.ymgme.2025.109259","DOIUrl":"10.1016/j.ymgme.2025.109259","url":null,"abstract":"<div><h3>Background</h3><div>Mitochondrial aminoacyl tRNA synthetase (mt-ARS) related disorders represent a widely heterogeneous group of diseases affecting the efficiency of mitochondrial protein synthesis.</div><div><em>AARS2</em> and <em>DARS2</em> biallelic mutations are associated with clinical syndromes prominently characterized by diffuse leukoencephalopathy with a highly variable age of onset, ranging from early infancy to adulthood.</div><div>Preliminary in vitro results on patients' fibroblasts and some anecdotal reports on patients affected by mt-ARS related disease have suggested a possible benefit of supplementation with the specific substrate amino acid of the defective mt-ARS.</div></div><div><h3>Methods</h3><div>We recruited 6 adult patients affected by <em>AARS2</em> (<em>n</em> = 2) and <em>DARS2</em> (<em>n</em> = 4) related leukoencephalopathies and started an oral supplementation with alanine and aspartate, respectively, for a total duration of 2 years. Therapeutic efficacy and safety were assessed through clinical examinations, standardized scales, functional tests, quality of life (QoL) scores, brain MRI, and laboratory analyses.</div></div><div><h3>Results</h3><div>Overall, the treatment was safe and well tolerated by all patients, but efficacy endpoints were not met as no significant improvements were observed in global, cognitive, or motor scores.; nonetheless, all patients but one remained clinically stable.</div></div><div><h3>Conclusions</h3><div>Despite inherent limitations of this pivotal trial, our findings suggest that specific amino acid supplementation is a safe intervention but do not yield a clear symptomatic benefit; nevertheless, we cannot exclude a potential role in stabilizing the clinical condition in adult patients with <em>DARS2</em>-related disorders.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 3","pages":"Article 109259"},"PeriodicalIF":3.5,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145270248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional ability profiles in beta-propeller protein-associated neurodegeneration (BPAN)","authors":"Francesco Gavazzi ,&nbsp;Samuel R. Pierce ,&nbsp;Vanessa Smith ,&nbsp;Eric Yang ,&nbsp;Julie Skorup ,&nbsp;Kristy Pucci ,&nbsp;Emma Kotes ,&nbsp;Allan M. Glanzman ,&nbsp;Stacy V. Cusack ,&nbsp;Todd Levy ,&nbsp;Holly Dubbs ,&nbsp;Emma Wiener ,&nbsp;Sarah Woidill ,&nbsp;Joseph Vithayathil ,&nbsp;Abbas Jawad ,&nbsp;Nivedita Thakur ,&nbsp;Laura A. Adang","doi":"10.1016/j.ymgme.2025.109253","DOIUrl":"10.1016/j.ymgme.2025.109253","url":null,"abstract":"<div><h3>Background</h3><div>Beta-propeller Protein-Associated Neurodegeneration (BPAN) is a rare neurodevelopmental degenerative disorder caused by pathogenic variants in <em>WDR45</em> leading to brain iron accumulation. Its rarity and complex clinical course make it difficult to select appropriate clinical outcome assessments (COAs). This study evaluates established COAs for feasibility and effectiveness in capturing BPAN's functional ability profiles exploring cognitive, motor, and behavioral features.</div></div><div><h3>Methods</h3><div>We performed an observational study. Children were recruited as part of the Myelin Disorders Biorepository Project at the Children's Hospital of Philadelphia. We administered the Gross Motor Function Measure-88 (GMFM-88), the Leiter International Performance Scale (Leiter-3), and the Vineland Adaptive Behavior Scale (VABS-3). A Rasch validated version of the GMFM-88, the GMFM-66, was derived from the GMFM-88 data. Descriptive statistics and Spearman's rank correlation were used to compare assessments. Statistical analyses were performed to compare performance across cohorts and assess correlations, with significance defined as <em>p</em> &lt; 0.05.</div></div><div><h3>Results</h3><div>Fifty-three individuals (43 females, 10 males) with molecularly confirmed BPAN participated. The VABS-3 (<em>n</em> = 53) showed a decline in adaptive skills over time, with significant differences between Communication and Socialization Domain performance (Kruskal-Wallis test with Dunn's correction <em>p</em> &lt; 0.0001). GMFM-88 assessments (<em>n</em> = 32) showed a median performance of 33.4 %. Patient participation/behavior affected data completeness. The more limited GMFM-66 correlated better with the VABS-3 Gross Motor subdomain than the GMFM-88 (<em>r</em> = 0.94, <em>r</em> = 0.73, respectively). The Leiter-3 (<em>n</em> = 36) demonstrated significant non-verbal cognitive impairment, although there were behavioral challenges which impacted implementation. Longitudinal VABS-3 data revealed a median − 2.9 points/year decline in Adaptive Behavior Composite scores, reflecting progressive functional loss.</div></div><div><h3>Discussion</h3><div>This study highlights key considerations for selecting COAs in BPAN. The panel of COAs should accommodate the behavioral challenges associated with BPAN that can limit participant compliance with testing. The abbreviated GMFM-66 was a more reliable tool to capture motor skills. Similarly, behavioral difficulties impacted Leiter-3 performance, which demonstrated general impairment in non-verbal cognitive skills. The VABS-3 effectively tracked adaptive function decline, demonstrating feasibility for longitudinal monitoring. Future studies should expand cohort size, refine assessment strategies, and align measures with disease progression to optimize clinical trial readiness.</div></div>","PeriodicalId":18937,"journal":{"name":"Molecular genetics and metabolism","volume":"146 3","pages":"Article 109253"},"PeriodicalIF":3.5,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145308484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}