Journal of Molecular Histology最新文献

{"title":"Ameliorative effects of chitosan on fluoride-induced kidney injury in rats: a stereological and immunohistochemical study","authors":"Fikret Altındağ,&nbsp;Uğur Özdek","doi":"10.1007/s10735-025-10428-0","DOIUrl":"10.1007/s10735-025-10428-0","url":null,"abstract":"<p>The present study aimed to investigate the possible protective effects of chitosan (CS) on fluoride-induced nephrotoxicity. 28 rats were divided into four groups (n = 7). The Control group received drinking water. Sodium fluoride (NaF) group received 100 mg/L NaF in drinking water. NaF + CS group received 100 mg/L NaF and 250 mg/kg/day CS by gastric gavage. CS group was given 250 mg/kg/day CS by gavage. The study period lasted 12 weeks. Total kidney volume, Bowman’s capsule volume, Bowman’s space volume, Tubular volume and Glomerulus volume were measured by stereological methods. Immunohistochemically, caspase-3 and TNF-alpha expressions were evaluated. Biochemically, levels of urea and creatinine were measured. In addition, a histopathological evaluation of the kidney was performed. According to the control group, an increase was observed in all stereological parameters except glomerulus volume in the NaF group. CS treatment inhibited the increase in stereological parameters. Fluoride increased expressions of caspase-3 and TNF-α in the kidney, and serum urea and creatine levels, but CS decreased these parameters. In addition, pathological changes in the kidney caused by fluoride such as tubular dilatation, enlargement of the Bowman’s space, and deterioration in tubular epithelial cells were restored with CS treatment. The conclusions of the current study reveal that fluoride can cause nephrotoxicity and CS treatment can prevent fluoride-induced nephrotoxicity.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143888767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Forsythoside A inhibited inflammatory response by inhibiting p38 JNK/MAPK/ERK and NF-κB signaling in Staphylococcus aureus pneumonia","authors":"Liangmin Song,&nbsp;Yu Lei","doi":"10.1007/s10735-025-10418-2","DOIUrl":"10.1007/s10735-025-10418-2","url":null,"abstract":"<div><h3>Background</h3><p><i>S. aureus</i> pneumonia, one of the most common <i>S. aureus</i>-induced diseases, is characterized by infectious inflammation in alveoli, distal airway, and lung interstitial. Forsythiaside A possesses anti-inflammatory, anti-infective, and other pharmacological properties in several diseases. The role of forsythiaside A remains unclear in <i>S. aureus</i> pneumonia.</p><h3>Aim of the study</h3><p>We aimed to figure out the role of forsythiaside A in <i>S. aureus</i> pneumonia.</p><h3>Methods</h3><p>RAW264.7 cells and C57BL6 mice were infected with <i>S. aureus</i> to construct <i>S. aureus</i> pneumonia cell model and animal model, respectively. A series of experiments including MTT, ELISA, Western blot, H&amp;E staining and EBD staining were operated to figure out the role of forsythiaside A in <i>S. aureus</i> pneumonia.</p><h3>Results</h3><p>In RAW264.7 cells, forsythiaside A did not induce cell toxicity but triggered cytokines (TNF-α, IL-6 and IL-1β) release in a dose-dependent manner. Moreover, forsythiaside A inhibited p38 JNK/MAPK/ERK and NF-κB pathways by repressing phosphorylation of p38, JNK, ERK and p65 proteins. For in vivo study, forsythiaside A improved survival rate of <i>S. aureus</i> pneumonia mice by alleviating lung injury. In addition, forsythiaside A protected from air-blood barrier destruction and pulmonary edema. At last, forsythiaside A inhibited neutrophils infiltration and inflammatory response in bronchoalveolar lavage fluid.</p><h3>Conclusions</h3><p>Forsythoside A inhibited inflammatory response by inhibiting p38 JNK/MAPK/ERK and NF-κB signaling in <i>S. aureus</i> pneumonia, which provided a novel insight for <i>S. aureus</i> pneumonia treatment.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143879742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"KIF2C promotes oral squamous cell carcinoma progression via PLK1 upregulation: implications for biomarker development and therapeutic targeting","authors":"Chenfei Wang,&nbsp;Yuyuan Su,&nbsp;Jinlong Shi,&nbsp;Guijuan Feng","doi":"10.1007/s10735-025-10415-5","DOIUrl":"10.1007/s10735-025-10415-5","url":null,"abstract":"<div><p>Oral squamous cell carcinoma (OSCC) is a highly aggressive malignancy with poor prognosis due to late detection, rapid progression, and frequent metastasis, underscoring the urgent need for novel therapeutic targets. This study investigates the roles of kinesin family member 2C (KIF2C) and Polo-like kinase 1 (PLK1) in OSCC progression and their functional interplay. Immunohistochemical and western blot analyses revealed marked upregulation of KIF2C and PLK1 in human OSCC tissues and cell lines (SCC9, SCC25, Cal27). Functional characterization in Cal27 cells (selected for highest KIF2C expression via qPCR/WB) demonstrated that KIF2C knockdown via siRNA transfection suppressed proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while inducing apoptosis and G0/G1 cell cycle arrest. Mechanistically, KIF2C silencing downregulated PLK1 expression, concomitantly reducing EMT markers (N-cadherin, vimentin), matrix metalloproteinases (MMP-2/9), and angiogenesis factors (VEGF, α-SMA). Complementary assays (CCK-8, EdU, Transwell, wound healing) and flow cytometry confirmed that KIF2C-PLK1 axis promotes tumor growth by enhancing matrix degradation, angiogenesis, and S-phase proliferation while inhibiting apoptosis. These findings establish KIF2C as a pivotal regulator of OSCC progression through PLK1-mediated signaling, highlighting their dual potential as prognostic biomarkers and therapeutic targets for OSCC management.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143879743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"STAT3/FoxO3a/Sirt1 pathway inhibition by ginsenoside Rc ameliorates cardiomyocyte damage in septic cardiomyopathy by altering macrophage polarization","authors":"M. S. Jinzhong Wang,&nbsp;M. S. Jian Fu","doi":"10.1007/s10735-025-10417-3","DOIUrl":"10.1007/s10735-025-10417-3","url":null,"abstract":"<div><p>This study explored the role and mechanism of action of ginsenoside Rc in treating septic cardiomyopathy. Ginsenoside Rc mitigated LPS-induced oxidative stress, inflammation, apoptosis, and mitochondrial dysfunction in cardiomyocytes and inhibited M1 polarization in macrophages. Ginsenoside Rc reduced the stimulating effect of M1-polarized macrophages on LPS-induced cardiomyocyte injury. Network pharmacological analysis suggested that ginsenoside Rc may play a role in septic cardiomyopathy through modulation of the STAT3/FoxO3a/Sirt1 pathway, which was validated in in vitro experiments. Ginsenoside Rc suppressed the expression of STAT3/FoxO3a pathway proteins and upregulated Sirt1. Moreover, influences of ginsenoside Rc on LPS-induced cardiomyocyte injury and macrophage polarization were abolished by ML115, a STAT3 agonist. In vivo, ginsenoside Rc notably improved myocardial injury and attenuated macrophage activation and inflammation in septic mice. Collectively, Ginsenoside Rc can ameliorate septic cardiomyopathy by modulating the STAT3/FoxO3a/Sirt1 pathway and altering macrophage polarization.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143883694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Green synthesis of silver and gold nanoparticles using seeds extract of Cichorium intybus and their comparative analysis with commercially available ointment for wound healing activity","authors":"Amna Khalid,&nbsp;Shazia Khurshid,&nbsp;Maliha Uroos,&nbsp;Jahangir Khan,&nbsp;Abid Sarwar,&nbsp;Ehsan ul Haq,&nbsp;Tariq Aziz,&nbsp;Fatma Alshehri,&nbsp;Fahad Al-Asmari,&nbsp;Bandar K. Baothman,&nbsp;Fakhria A. Al-Joufi,&nbsp;Maher S. Alwethaynani","doi":"10.1007/s10735-025-10426-2","DOIUrl":"10.1007/s10735-025-10426-2","url":null,"abstract":"<div><p>Wound healing is a complicated physiological process that involves several stages including hemostasis, inflammation, proliferation and repair to rebuild the integrity of the skin and subcutaneous tissue. Millions of people around the world are affected by poor wound healing, causing increased mortality rates and related costs. Immedicable wounds are a health problem because they directly affect the person’s standard of living and produce an ultimatum to the health of people and the international economy because of the expensive medical treatment. Other schemes/approaches must be designed to achieve productive and therapeutic results. In this context, the emergence of Nano biotechnology may provide another manifesto to produce latest drugs for long-term treatment processes. This article shows that the implementation of metal nanoparticles (Au and Ag) has unbolted a brand-new gateway in the discipline of eco-friendly medicine due to their unique properties such as medicine transportation, antimicrobial activity and quick recovery. Moreover, metal nanoparticles (NPs) manufactured by green synthesis not only add the effects of nanoparticles and plant extracts but also reduce toxicity to tissues and make their use safer. In the present work, Ag and Au nanoparticles were synthesized using an aqueous seed extract of <i>Cichorium intybus</i> and their wound healing ability was assessed by performing in-vivo wound healing activity on albino mice. Till now there is no study available on the in-vivo wound healing potential of Ag and Au nanoparticles using <i>Cichorium intybus</i>. This is the first study ever to assess the ability of <i>Cichorium intybus</i> seed extract and its metal nanoparticles (AgNPs &amp; AuNPs) to promote wound healing in animals which shows its uniqueness and novelty. The results displayed augmented and quicker wound closure with Ag as compared to the Au nanoparticles, polyfax and simple plant extract in a 21-day research work. These results illustrated that eco-friendly prepared nanoparticles provide a prominent approach to fight with the bacteria resistant against combination therapy without any lethal affair. Environment-friendly NPs declared to be the low-cost best treatment for the faster recovery of wounds. The main goal of this research is to provide aid in the creation of plant-based, durable and affordable Nano medicine for wound care, lowering dependency on synthetic techniques and encouraging environmental friendly biomedical applications.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143875313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of the oncogenic role of centromere protein M in non-small cell lung cancer via CDC20/MYBL2/Wnt signaling pathways","authors":"Ling Wu,&nbsp;Jun Li,&nbsp;Haoyu Wang,&nbsp;Xu Chang,&nbsp;Qinglong Kong","doi":"10.1007/s10735-025-10423-5","DOIUrl":"10.1007/s10735-025-10423-5","url":null,"abstract":"<div><p>Lung cancer remains the most prevalent carcinoma with a high mortality rate, yet the underlying mechanisms driving pulmonary neoplasia and disease progression are not fully understood. In our study, we conducted a comprehensive analysis of the transcriptome profiles and clinicopathological characteristics of 515 patients diagnosed with non-small cell lung cancer (NSCLC) from the TCGA database. We identified a significant upregulation of centromere protein M (CENPM) in NSCLC tissues, which was positively correlated with poor prognosis. Furthermore, overexpression of CENPM markedly promoted cell proliferation and increased the tumorigenic potential of NSCLC cell lines (A549/NCI-H1299), leading to accelerated tumor progression and reduced survival time in tumor-bearing mice. Mechanistically, CENPM activated the Wnt/β-catenin signaling pathway via the cell division cycle 20 (CDC20)/MYB proto-oncogene-like 2 (MYBL2) axis. Inhibition of either Wnt signaling or the CDC20/MYBL2 axis attenuated the tumorigenic potential and proliferative effects induced by CENPM. Our findings underscore the critical role of CENPM in driving NSCLC development and suggest that CENPM could serve as a novel biomarker for predicting NSCLC progression in clinical settings.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-025-10423-5.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143875314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vildagliptin topical ointment: an effective treatment for imiquimod-induced psoriasis in mice","authors":"Basma Farooq Ali,&nbsp;Ahmed Rahmah Abu-Raghif,&nbsp;Hayder Ridha-Salman,&nbsp;Ali Jihad Hemid Al-Athari","doi":"10.1007/s10735-025-10416-4","DOIUrl":"10.1007/s10735-025-10416-4","url":null,"abstract":"<div><p>Psoriasis is a chronic immune-related dermatosis characterized by inflamed, thickened, brownish-red, peeling skin patches. Vildagliptin is an anti-diabetic drug with novel anti-inflammatory, anti-oxidative, and anti-proliferative activities. This study aimed to assess the anti-psoriatic activity of topical vildagliptin. 40 Swiss albino mice were sorted into five groups, each with 8 animals. The control group obtained no treatment. The induction group obtained imiquimod cream (5%) at a dose of 62.5 mg per day. The vehicle group obtained imiquimod (as did the induction group), accompanied by topical vehicle application. The clobetasol group obtained imiquimod cream (as did the induction group), and two hours later, clobetasol ointment (0.05%) was administered. The vildagliptin group obtained imiquimod (as in the induction group), followed by topical vildagliptin ointment (3%), two hours after induction. The experiment lasts for 8 consecutive days. Evaluations were conducted on the results of biochemical indicators, histological assessments, and clinical observations. Vildagliptin administered topically effectively corrected psoriatic histological irregularities, improved the psoriasis-like skin lesions such as erythema, flacking, and acanthosis, and attenuated the imiquimod-provoked elevations of PASI and Baker’s score. Further, overexpression of inflammatory markers (TNF-α, IL-17 A, IL-23, and IL-22), angiogenic markers (VEGF), oxidative-stress components (MDA and SOD), and proliferative factors (Ki-67) were dramatically mitigated by vildagliptin treatment. Topical vildagliptin has profound anti-psoriatic effects.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143875315","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: The Sirt1/FOXO signal pathway involves in regulating osteomyelitis progression via modulating mitochondrial dysfunctions and osteogenic differentiation","authors":"Runyao Zhang,&nbsp;Nannan Kou,&nbsp;Feifei Liu,&nbsp;Huan Tong,&nbsp;Shaobo Li,&nbsp;Lirong Ren","doi":"10.1007/s10735-025-10422-6","DOIUrl":"10.1007/s10735-025-10422-6","url":null,"abstract":"","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of mitochondrial dysfunction on placental trophoblastic cells in intrahepatic cholestasis of pregnancy","authors":"Xiaomei Huang,&nbsp;E. Liao,&nbsp;Aixing Chen,&nbsp;Yong Shao","doi":"10.1007/s10735-025-10427-1","DOIUrl":"10.1007/s10735-025-10427-1","url":null,"abstract":"<div><p>Intrahepatic cholestasis of pregnancy (ICP) is a pregnancy-specific disorder characterized by elevated serum bile acids and adverse fetal outcomes. Elevated bile acids can lead to excessive accumulation of reactive oxygen species (ROS) in the placenta, and high ROS levels can cause mitochondrial damage. This study primarily investigates the mechanisms of bile acid-induced mitochondrial dysfunction to provide precise targets for the treatment of ICP. Single-cell sequencing of human placental tissues was conducted to analyze changes in mitochondrial function of ICP placental trophoblasts. An ICP cell model was established using TCA, and the effects of TCA on trophoblast mitochondrial function were observed through detection of ROS, mitochondrial membrane potential, fluorescence confocal microscopy, and other methods. Single-cell sequencing indicated significant impairment of mitochondrial function in ICP placental trophoblasts, and electron microscopy results also suggested severe damage to the mitochondrial structure of ICP placental trophoblasts. Both the morphology and function of mitochondria in the ICP cell model were significantly altered, possibly due to impaired mitochondrial transcription mechanisms mediated by NRF1/PGC-1α pathway. Elevated serum bile acids in ICP pregnant women may lead to mitochondrial damage in placental trophoblasts through the NRF1/PGC-1α pathway, thereby affecting the function of placental trophoblasts.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871347","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nobiletin ameliorates hormone-induced osteoblast apoptosis by modulating JAK2/STAT3 signaling","authors":"Xiang Li,&nbsp;Yuanzhen Bai,&nbsp;Jia Tong,&nbsp;Guoqing Mao","doi":"10.1007/s10735-025-10424-4","DOIUrl":"10.1007/s10735-025-10424-4","url":null,"abstract":"<div><p>Our paper aimed to disclose the effects of nobiletin (NOB) on hormone-induced osteoblast apoptosis and potential action mechanism. MC3T3-E1 cells were randomly separated into normal group, glucocorticoid (GC) group, L-NOB group, M-NOB group, H-NOB group, and Colivelin group (Colivelin: JAK2/STAT3 activator). CCK-8 was applied to ascertain the activity of MC3T3-E1 cells. FITC-Annexin V/PI method was applied to measure cell apoptosis. Alkaline phosphatase (ALP) assay kit was applied to measure ALP activity. Enzyme linked immunosorbent assay (ELISA) was implemented to ascertain the levels of IL-6, IL-1β, TNF-α, and ROS. Western blotting was implemented to distinguish the expressions of JAK2/STAT3 pathway proteins. The viability of MC3T3-E1 cells, ALP activities, and bcl-2 protein level were considerably decreased, while the apoptotic rate, the levels of TNF-α, IL-1β, IL-6, ROS, and the expressions of pJAK2/JAK2, pSTAT3/STAT3, Caspase-3, and bax proteins were greatly increased in each group after GC treatment. In comparison with GC group, MC3T3-E1 cell viability, ALP activity, and bcl-2 protein level in the L-NOB group, M-NOB group, and H-NOB group were greatly increased. Conversely, the apoptotic rate, the levels of TNF-α, IL-1β, IL-6, ROS, and the expressions of pJAK2/JAK2, pSTAT3/STAT3, Caspase-3, and bax proteins were markedly reduced. In contrast to H-NOB group, the apoptotic rate, the levels of TNF-α, IL-1β, IL-6, ROS, and the expressions of pJAK2/JAK2, pSTAT3/STAT3, Caspase-3, and bax proteins in Colivelin group were considerably enhanced, while MC3T3-E1 cell viability, ALP activity, and bcl-2 protein level were greatly declined. NOB ameliorates hormone-induced osteoblast apoptosis by reducing JAK2/STAT3 signaling activity.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-025-10424-4.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143871348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}