Journal of Molecular Histology最新文献

{"title":"Upregulation of Caspase-3 and TNF-α in a rat model of cerebellar motor disorder: role of Cucumis sativus (cucumber).","authors":"Osagie Usman Idemudia, Adaze Bijou Enogieru","doi":"10.1007/s10735-025-10482-8","DOIUrl":"https://doi.org/10.1007/s10735-025-10482-8","url":null,"abstract":"","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":"191"},"PeriodicalIF":2.9,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144257065","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":"Role and mechanism of lncRNA ZEB1-AS1 endogenous competition for miR-365a-3p targeting NRF2 in ferroptosis in articular chondrocytes.","authors":"RenBo Zhang, YuYan Liu, Hui Zang, Axiang He, YanJie Mao, WanJun Liu","doi":"10.1007/s10735-025-10450-2","DOIUrl":"https://doi.org/10.1007/s10735-025-10450-2","url":null,"abstract":"<p><p>Osteoarthritis (OA) is an extremely complex chronic whole joint disease. The regulation of NRF2 in cellular ferroptosis is involved in OA development; however, its upstream regulatory mechanism is unclear. Long noncoding RNAs (lncRNAs) regulate the expression of downstream target genes through endogenous competition with micro RNAs. LncRNA ZEB1-AS1 regulates the expression of miR-365a-3p, which in turn negatively regulates NRF2 expression. Both lncRNA ZEB1-AS1 and NRF2 can bind to miR-365a-3p at the same target site. However, it remains unclear whether ZEB1-AS1 could act as a competing endogenous RNA (ceRNA) to reduce miR-365a-3p-mediated inhibition of NRF2. Specifically, the potential mechanism whereby ZEB1-AS1 might sequester miR-365a-3p through competitive binding, thereby alleviating its suppressive effect on NRF2 expression, requires further experimental validation. Therefore, our study aimed to investigate whether lncRNA ZEB1-AS1 could participate in the regulation of NRF2 expression through endogenous competition for binding to miR-365a-3p, as well as the role and mechanism in osteoarthritic cellular ferroptosis. Our findings demonstrated that NRF2 knockdown combined with miR-365a-3p overexpression significantly enhanced cellular ferroptosis and accelerated osteoarthritis progression. Conversely, both miR-365a-3p inhibition and ZEB1-AS1 overexpression were found to upregulate NRF2 expression, thereby mitigating cellular ferroptosis and OA development. Notably, ZEB1-AS1 overexpression exerted dual protective effects in chondrocytes by elevating NRF2 levels, effectively suppressing both ferroptosis and inflammatory damage. Mechanistically, we identified that the lncRNA ZEB1-AS1 modulates OA pathogenesis through the miR-365a-3p/NRF2 axis, suggesting this pathway may serve as a potential therapeutic target for early intervention in OA progression.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":"190"},"PeriodicalIF":2.9,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144245583","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":"Maternal high-fat diet impairs cognitive performance by altering hippocampal GRP78/PERK axis and BDNF expression in adult female rat offspring: the potential protective role of N acetylcysteine.","authors":"Elfide Gizem Bakirhan, Elif Merve Betül Yanilmaz, Kıymet Kübra Tüfekci, Furkan Bakirhan, Solmaz Susam","doi":"10.1007/s10735-025-10471-x","DOIUrl":"https://doi.org/10.1007/s10735-025-10471-x","url":null,"abstract":"<p><p>Maternal high fat diet (HFD) affects the neurodevelopment of offspring and has long-term consequences on cognitive behavior. This study investigated changes occurring in GRP78 and PERK, important markers of endoplasmic reticulum stress (ERS) signaling, in the hippocampus of female adult rats exposed to maternal HFD, and in brain-derived neurotrophic factor (BDNF) signaling, with its important role in the regulation of cognitive behavior, and the potential neuroprotective effects of N-acetylcysteine ​​(NAC) against these changes. A maternal obesity model was created with HFD (60% kcal). NAC (150 mg/kg) was administered intragastrically to both the NAC and HFD + NAC groups. The animals were mated at 12 weeks of age. The same diet was maintained throughout pregnancy and lactation. All female rat pups were subjected to the water maze test at eight weeks of age. Hippocampal GRP78 and PERK expressions increased in the HFD rats. However, maternal HFD suppressed hippocampal BDNF levels and reduced hippocampal neuronal volume. NAC supplementation reduced GRP78 and PERK expressions and increased BDNF and hippocampal volume values ​​in the HFD + NAC group. At behavioral assessments, rats in the HFD group exhibited decreased memory and learning ability, but the HFD + NAC group exhibited stronger responses than the HFD group. Our findings suggest that the decrease in BDNF expression, which plays a role in memory and learning, after maternal HFD exposure may be due to ERS associated with increased GRP78 and PERK expressions. Furthermore, NAC supplementation may ameliorate the impairment in memory and spatial learning ability by attenuating hippocampal ERS in HFD rats.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":"189"},"PeriodicalIF":2.9,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144245582","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":"The mechanism of promoting angiogenesis after cerebral infarction by scalp acupuncture based on MATN2/WNT3a/β-catenin.","authors":"Qian Zhang, Shengwang Han, Yi Zheng, Jiayuan Li, Le Ma, Jinlang Tan, Xingyu Kang, Rui Gong, Siyu Chen, Shuai Shi","doi":"10.1007/s10735-025-10461-z","DOIUrl":"https://doi.org/10.1007/s10735-025-10461-z","url":null,"abstract":"<p><p>Scalp acupuncture, a therapeutic modality derived from traditional acupuncture theory, has been widely applied in clinical practice for cerebral infarction management in China. In this study, a middle cerebral artery occlusion (MCAO) rat model was established. Therapeutic efficacy was evaluated through multidimensional approaches: (1) Neurological functional assessment using modified Neurological Severity Score (mNSS); (2) Quantitative infarct volume measurement via 2,3,5-triphenyltetrazolium chloride (TTC) staining; (3) Histopathological analysis through hematoxylin-eosin (HE) staining. Additional analytical techniques including transmission electron microscopy (TEM) and immunofluorescence staining were employed to investigate the expression patterns of MATN2, WNT3a, β-catenin, and CD34 biomarkers, elucidating the potential mechanisms underlying scalp acupuncture-induced angiogenesis post-cerebral infarction in animal models. Key findings included: marked reduction in mNSS scores at 1-day and 7-day post-intervention intervals (P < 0.01); substantial decrease in cerebral infarction volume quantified by TTC staining (P < 0.05); enhanced neuronal density and preserved cytoarchitectural integrity in peri-infarct regions observed through HE staining. Ultrastructural analysis via TEM revealed notable improvements in microvascular endothelial cell (EC) morphology and intercellular junctions. Immunofluorescence quantification showed upregulated expression of pro-angiogenic factors MATN2, WNT3a, and β-catenin, accompanied by increased CD34 + microvascular density (P < 0.01). This study provides comprehensive experimental evidence that scalp acupuncture administration facilitates post-ischemic angiogenesis, suggest potential therapeutic applications for stroke rehabilitation.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":"186"},"PeriodicalIF":2.9,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144223895","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":"Knockout of the Staphylococcus aureus virulence gene sdrC promotes Myh7 expression to inhibit the progression of osteomyelitis.","authors":"Baochuang Qi, Lili Yang, Xinyu Fan, Dongdong Qin, Jiming Gan, Tao Chen, Yu Rao, Zhongyu Peng, Longjun Su, Chuan Li, Yongqing Xu","doi":"10.1007/s10735-025-10447-x","DOIUrl":"https://doi.org/10.1007/s10735-025-10447-x","url":null,"abstract":"<p><p>The incidence of osteomyelitis has been increasing annually, but the specific molecular pathogenesis of Staphylococcus aureus-induced osteomyelitis is unclear. The SdrC protein facilitates Staphylococcus aureus adhesion and colonization, thereby promoting subsequent biofilm accumulation and contributing to the progression of osteomyelitis. The role of SdrC, an important protein in S. aureus, in the progression of S. aureus-induced osteomyelitis requires further elucidation. Thus, we aimed to determine whether targeting SdrC is a novel strategy for treating S. aureus-induced osteomyelitis. The sdrC sequence of S. aureus was knocked out, and rat models with wild-type and sdrC knockout (KO) S. aureus-induced osteomyelitis were established. Enzyme-linked immunosorbent assays (ELISAs) were used to identify differences in the levels of the inflammatory factors IL-6 and TNF-α, and qPCR and Western blotting were used to identify changes in the levels of osteogenic indicators, such as ALP, OST and Runx2; these experiments analyzed the role of SdrC in the progression of S. aureus-induced osteomyelitis. Transcriptomic sequencing was used to explore the mechanism by which SdrC promotes the development of S. aureus-induced osteomyelitis at the molecular level. After the SdrC protein of S. aureus was knocked out, biofilm formation significantly decreased. Compared with the control group, The sdrC-KO osteomyelitis group showed milder bone tissue inflammation compared to the control group, and the expression of the inflammatory factors IL-6 and TNF-α decreased significantly (p < 0.05), whereas the expression of the osteogenic indicators ALP, OST, and Runx2 increased significantly, as shown by qPCR and Western blotting (p < 0.05). Alkaline phosphatase and alizarin red staining showed that knocking out SdrC increased ossification in rats and improved their prognosis. Transcriptomic sequencing revealed that Myh7 was significantly overexpressed in the sdrC-KO rats with osteomyelitis (p < 0.05). Knocking out Myh7 significantly reduced the mRNA and protein levels of osteogenic markers Runx2, ALP, Osterix (OSX), and osteocalcin (p < 0.05), suggesting that Myh7 inhibits the function of the S. aureus SdrC protein. The SdrC protein in S. aureus promotes the malignant progression of osteomyelitis and exacerbates the development of osteomyelitis by promoting S. aureus biofilms. Moreover, Myh7 hinders the ability of SdrC to promote biofilm formation, reducing the progression of osteomyelitis; these findings suggest that targeting SdrC or enhancing Myh7 expression could serve as a novel therapeutic strategyjbr osteomyelitis treatment.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":"185"},"PeriodicalIF":2.9,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144223971","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":"Mitigation of cadmium-induced hepatotoxicity by orally administered Xylopia aethiopica synthesized silver nanoparticles in rats.","authors":"Emmanuel Nnaemeka Uhuo, Chiemeziem Adnma Obike, Parker Elijah Joshua, Prince Ogochukwu Alaebo, Rhonick Chukwuemeka Anyanwu","doi":"10.1007/s10735-025-10454-y","DOIUrl":"https://doi.org/10.1007/s10735-025-10454-y","url":null,"abstract":"<p><p>Cadmium is a major environmental pollutant that results in hepatic necrosis by mediating oxidative stress and inflammation. Xylopia aethiopica is a natural plant that has been reported to have a wide range of pharmacological properties. The study aimed at determining the ameliorative potential of Xylopia aethiopica synthesized silver nanoparticles (Xa-AgNPs) against hepatotoxicity induced by cadmium in rats. Thirty male Wistar rats were randomly grouped into six (n = 5). I: served as control, II: received 10 mg/kg of silymarin only, III, IV, V, and VI were given 20 mg/kg b.wt of cadmium chloride (CdCl₂) orally for seven consecutive days. After which, IV, V, and VI were treated with 10 mg/kg bwt of silymarin, 5 and 10 mg/kg Xa-AgNPs consecutively for 21 days. Synthesized silver nanoparticles were characterized. Biomarkers were determined as well as histological examination. X-ray diffraction revealed that the structure of silver nanoparticles is spherical and polydispersed. Scanning electron microscope confirmed the spherical nature, size and, the crystallinity of nanoparticles. The average size of nanoparticles, 2.13 nm, was recorded. Oral administration of CdCl₂ caused significant (p < 0.05) increase of alanine transaminase (ALT) and aspartate aminotransferase (AST), arginase, serum albumin, and γ-glutamyl transferase (GGT) activities compared with normal control. Also, malondialdehyde (MDA) increased in Cd-induced only against treatment groups. Conversely, administration of 10 mg/kg of Xa-AgNPs and silymarin respectively reversed these changes with significant (p < 0.05) reduction of MDA, ALT and elevation of serum albumin, increase activities of superoxide dismutase (SOD), and catalase(CAT) in test groups against Cd-induced only. Similarly, arginase, and GGT activities increased in test groups compared with the Cd-induced only. Therefore, it can be ascertained that Xa-AgNPs ameliorate Cd-induced hepatotoxicity in rats.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":"187"},"PeriodicalIF":2.9,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144223893","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":"MiR-1293 modulates PPARGC1A to promote proliferation and metastasis of oral carcinoma cells.","authors":"Qian Zhou, Xin Zhang","doi":"10.1007/s10735-025-10474-8","DOIUrl":"https://doi.org/10.1007/s10735-025-10474-8","url":null,"abstract":"<p><p>We aimed to assess the influence of microRNA-1293 (miR-1293) on the proliferation and metastasis of oral carcinoma cells through modulating peroxisome proliferator-activated receptor γ coactivator 1α (PPARGC1A). Carcinoma and para-carcinoma control tissues were sampled from 60 patients with oral carcinoma to measure the expression of miR-1293 and analyze its associations with clinicopathological characteristics. Then qRT-PCR was performed for detecting miR-1293 and PPARGC1A mRNA expressions in oral carcinoma tissues and cells, and Western blotting was conducted to determine PPARGC1A protein expression. The luciferase activity of PPARGC1A-WT significantly dropped, PPARGC1A mRNA and protein expressions reduced, while proliferation, migration, invasion and viability were enhanced in the miR-1293 mimic group compared to the NC mimic group. The miR-1293 mimic + oePPARGC1A group had significantly weaker cell viability and smaller numbers of proliferative, migrating and invasive cells than those of the miR-1293 mimic + oeNC group. The anti-miR-1293 group, in comparison to the anti-NC group, had slower tumor growth in mice, increased mRNA and protein expressions of PPARGC1A in tumor tissues, as well as reduced tumor volume and weight, expression of miR-1293 and degree of tumor malignancy. MiR-1293 facilitates oral carcinoma cell proliferation and metastasis by suppressing the expression of PPARGC1A.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":"188"},"PeriodicalIF":2.9,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144223892","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":"Quercetin mitigates sepsis-induced renal injury via inhibiting inflammatory and oxidative pathways in mice.","authors":"Abdulla Kadhim Raheem, Ahmed Rahmah Abu-Raghif, Alaa Hamza Abbas, Hayder Ridha-Salman, Enass Najem Oubaid","doi":"10.1007/s10735-025-10442-2","DOIUrl":"https://doi.org/10.1007/s10735-025-10442-2","url":null,"abstract":"","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":"184"},"PeriodicalIF":2.9,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144223894","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":"RBM15 promotes m6A methylation and stability of KLF6 mRNA to accelerate pyroptosis of retinal ganglion cells in early-stage diabetic retinopathy.","authors":"Liqiong Zhou, Chunhui Zhang, Quan Cheng, Minjun Ma, Xinyu Fan, Yuanhui Han, Xu Zha, Yuanping Zhang","doi":"10.1007/s10735-025-10458-8","DOIUrl":"https://doi.org/10.1007/s10735-025-10458-8","url":null,"abstract":"<p><p>Neurodegeneration in early-stage diabetes retinopathy (DR) is mainly caused by the loss of retinal ganglion cells (RGCs), and high glucose-treated cell pyroptosis contributes to an important cause. However, the detailed molecular regulatory mechanism has not yet been thoroughly examined. In this study, primary mouse RGCs were stimulated with different concentrations of glucose, and mouse was intraperitoneally injected with streptozotocin (STZ) to construct DR model in vitro and in vivo. We found that compared to normal controls, RNA binding motif protein 15 (RBM15) was significantly upregulated in high glucose-treated RGCs and STZ-induced mice. RBM15 silence restored cell viability and inhibited cell apoptosis and cell death in high glucose-triggered RGCs. In parallel, RBM15 knockdown distinctly improved pathological damage such as thinning of retinal tissue thickness and loss of RGCs in STZ-modeling mice. Interestingly, the production of inflammatory cytokines and the expression of Cleaved caspase-1, NLRP3 and GSDMD-N were significantly reduced by RBM15 silence in vivo and in vitro. Mechanistically, RBM15 bound to kruppel like factor 6 (KLF6) mRNA to promote m6A modification and stabilize KLF6 mRNA, upregulating KLF6 expression in model cells and model mice retinal tissues. KLF6 overexpression increased the production of inflammatory cytokines and the expression of proteins related to pyroptosis, reversing the protective effects of RBM15 silence in high glucose-treated RGCs and diabetic retina. In conclusion, RBM15 is upregulated by high glucose, and stabilizes KLF6 mRNA to activate NLRP3-mediated pyroptosis pathway, exacerbating inflammation and apoptosis of RGCs and accelerating the progression of DR.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":"183"},"PeriodicalIF":2.9,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144214579","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":"Perinatal nicotine-induced neurotoxicity and behavioral alterations in newborn mice are associated with oxidative stress, inflammation and downregulated Nrf2/HO-1 signaling: protective role of Anethum graveolens.","authors":"Saleh Maodaa, Jamaan S Ajarem, Reem S Alruhaimi, Ahmed A Allam, Naif G Altoom, Ayman M Mahmoud","doi":"10.1007/s10735-025-10457-9","DOIUrl":"https://doi.org/10.1007/s10735-025-10457-9","url":null,"abstract":"<p><p>Perinatal exposure to nicotine has been implicated in causing significant oxidative stress and long-term neurobehavioral abnormalities. This study explores, for the first time, the efficacy of Anethum graveolens (dill) extract in mitigating neurotoxicity, oxidative damage, inflammation, and behavioral disturbances in neonatal mice exposed to nicotine during the perinatal period. Pregnant mice were administered 50 mg/kg of A. graveolens extract orally from gestational day 1 (GD1) to postnatal day 15 (PD15), alongside subcutaneous injections of nicotine (0.25 mg/kg) from GD12 to PD15. Nicotine-exposed neonates exhibited delayed developmental milestones (eye opening and hair growth), impaired neuromotor functions (righting, rotating, and cliff avoidance reflexes), and heightened anxiety-like behaviors. Nicotine induced substantial tissue damage, elevated levels of reactive oxygen species (ROS), malondialdehyde (MDA), and pro-inflammatory cytokines, and suppressed glutathione (GSH) levels and antioxidant enzyme activities across different brain regions (cerebrum, cerebellum, and medulla oblongata). A. graveolens extract improved developmental markers, restored neuromotor functions, reduced anxiety-like behaviors, and attenuated oxidative stress and inflammation. Moreover, it enhanced antioxidant defenses and upregulated the expression of Nrf2 and heme oxygenase-1 (HO-1). These findings indicate that A. graveolens exerts a protective role against nicotine-induced neurotoxicity by modulating oxidative and inflammatory responses and attenuating neurobehavioral alterations.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":"179"},"PeriodicalIF":2.9,"publicationDate":"2025-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144197982","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}