Histochemistry and Cell Biology最新文献

{"title":"August in focus in HCB: biomarker expression in specific tumor cell types.","authors":"Douglas J Taatjes, Jürgen Roth","doi":"10.1007/s00418-026-02542-1","DOIUrl":"https://doi.org/10.1007/s00418-026-02542-1","url":null,"abstract":"","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149193277","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":"Hormonal regulation of mitochondrial dynamics- and mitophagy-related marker expression in the endometrium and placenta.","authors":"Zehra Sezer, Umit A Kayisli, Semen Önder, İsmail Cepni, Timucin Timuroglu, Elif Guzel Meydanlı","doi":"10.1007/s00418-026-02544-z","DOIUrl":"https://doi.org/10.1007/s00418-026-02544-z","url":null,"abstract":"<p><p>Mitochondrial dynamics and mitophagy are indispensable for cellular homeostasis in hormonally regulated tissues such as the endometrium and placenta. Decidualization of endometrial stromal cells (ESCs) into decidual cells (DCs) requires extensive mitochondrial remodeling, yet how ovarian steroids regulate this process in vivo and in vitro remains incompletely understood. This study elucidates the modulation of mitochondrial fusion, fission, and mitophagy by estrogen (E2) and progesterone (P4) across the menstrual cycle and during pregnancy. Endometrial tissues were collected from women at early (EP) and late (LP) proliferative, and early (ES), mid (MS), and late (LS) secretory phases, while placental tissues were obtained from first-trimester (FP) and term pregnancies (TP). The expression of MFN2 and OPA1 (fusion), Drp1, Fis1, and MFF (fission), and Pink1 and Parkin (mitophagy) was assessed by immunohistochemistry in vivo. In vitro, the effects of E2 and P4 on these markers were examined in ESCs and DCs using western blotting. Mitochondrial morphology was evaluated by transmission electron microscopy and morphometry. In vivo, FP-DCs exhibited increased expression of fission- and mitophagy-related proteins, while in vitro P4 treatment was associated with increased Drp1 expression in FP-DCs. Collectively, these findings suggest that mitochondrial dynamics- and mitophagy-related protein changes accompany ESC-to-DC differentiation, with P4-associated Drp1 regulation potentially contributing to early pregnancy adaptation. Understanding these processes may provide insight into mechanisms relevant to implantation failure and pregnancy loss.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149180798","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":"Dexamethasone suppresses the sox3 gene during tail regeneration in the electric black ghost knifefish, Apteronotus albifrons (Linnaeus 1766).","authors":"Ammar A Issa, Ilham J J Alshami, Hutheyfa Al-Salih, Hussein A Saud, Christian Hacker, Maryam Alenize","doi":"10.1007/s00418-026-02538-x","DOIUrl":"10.1007/s00418-026-02538-x","url":null,"abstract":"<p><p>This study investigated the effects of different doses of dexamethasone on the regeneration of muscle fibers, electric organ cells, and electroreceptors in the amputated tails of the black ghost knifefish, Apteronotus albifrons (Linnaeus 1766). The relative gene expression of sox3 was analyzed to assess neural regeneration. Four groups of fish were exposed to dexamethasone concentrations of 0 (control), 1, 2, and 3 mg/L, with water replaced every 48 h to maintain drug stability. The results revealed that dexamethasone significantly downregulated sox3 expression. A significant decrease (p < 0.05) in relative expression levels was observed at the 1, 2, and 3 mg/L doses (0.134 ± 0.022, 0.061 ± 0.034, and 0.003 ± 0.002, respectively) compared to the control group (0.920 ± 0.252). These findings were supported by histological sections, which showed a reduced regeneration rate and lower growth percentages of neural and muscle tissues. Specifically, the neural tissue regeneration percentages were 28.40%, 14.80%, and 10.10% for the 1, 2, and 3 mg/L treatments, respectively. Transmission electron microscopy (TEM) revealed clear changes in the cellular organelles of the treated fish. These included a decrease in plasma membrane thickness, increased numbers of nuclei and mitochondria, enlarged vacuoles, and cell nucleus divisions. The treated fish also exhibited an increased count and clumping of red blood cells, which lost their normal discoid morphology and sometimes lacked nuclei. In conclusion, dexamethasone impairs the tissue regeneration process by inhibiting the growth of the electric organ, neurons, and intracellular organelles.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136229","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":"Deletion of Cipc promotes regenerative myogenesis in mdx mice and is associated with increased myogenin expression.","authors":"Ting Xue, Yu Zhao, Jianhua Wang, Yanfei Xu, Zhun Gu, Jiqing Zheng","doi":"10.1007/s00418-026-02543-0","DOIUrl":"10.1007/s00418-026-02543-0","url":null,"abstract":"<p><p>Skeletal muscle regeneration depends on satellite cells, which proliferate, differentiate, and fuse to repair damaged myofibers. Satellite-cell dysfunction contributes to defective regeneration in Duchenne muscular dystrophy (DMD), but the contribution of circadian regulators to this process remains incompletely understood. Here, we investigated the role of the CLOCK-interacting protein CIPC in satellite-cell differentiation and muscle regeneration in mdx mice. Satellite cell-specific deletion of Cipc increased centrally nucleated fibers and embryonic myosin heavy chain-positive regenerating fibers in dystrophic and ischemia-reperfusion-injured tibialis anterior muscles, and enhanced MyHC-positive myotube formation in primary cultures. Cipc deletion was accompanied by increased MyoD and myogenin mRNA expression and a higher number of myogenin-positive cells. RNA sequencing of day-3 differentiated satellite cells identified Mapk14/p38α and Elk1 as candidate upstream regulators associated with increased myogenin expression. Immunoblotting in three independent experiments further showed increased p38 and ELK-1 phosphorylation in Cipc-deficient satellite cells, without an apparent genotype-dependent change in total p38 or total ELK-1 abundance. These findings indicate that Cipc deletion enhances regenerative myogenesis in mdx mice and is associated with increased p38/ELK-1 signaling and myogenin expression. Because pathway inhibition, ELK-1 promoter-occupancy, and myogenin loss-of-function experiments were not performed, the p38/ELK-1-myogenin axis should be regarded as a candidate mechanism rather than an established causal pathway.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149108852","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":"Thorough formalin fixation confers a protective effect for histochemical and immunohistochemical testing on tissues exposed to prolonged time in ethanol, xylene, heat, or paraffin.","authors":"Rachelle Honeywell, Maggie Donner, Sheila Criswell","doi":"10.1007/s00418-026-02545-y","DOIUrl":"10.1007/s00418-026-02545-y","url":null,"abstract":"<p><p>Tissue under- and over-processing in the histology laboratory, while decreasing in frequency, is still a valid concern and typically results from user or instrument error. This study evaluated the effects of extended exposure of histological tissues to processing reagents on specimen quality, including embedding, microtomy, histochemical staining, and immunohistochemistry (IHC). All specimens were fixed in neutral buffered formalin for 3-5 weeks prior to processing except for a subset of organs which underwent prolonged fixation for 1 year. Although overprocessing is traditionally associated with tissue hardening, brittleness, and shrinkage, these effects are often noted when fixation timing is not clearly defined. To simulate processing delays, specimens were subjected to an additional 24 h in absolute ethanol, xylene, molten paraffin, or a heated embedding station. Extended exposure to these reagents did not result in observable morphologic changes. Embedding quality, microtomy performance, and histochemical staining were consistent across all experimental conditions. Additionally, IHC antigenicity was largely preserved under most conditions. However, reduced or absent immunoreactivity was observed in select markers in organs fixed for 1 year, consistent with prior reports of fixation-related antigen masking and deterioration of antigenic sites. Unexpectedly, extended exposure to ethanol, xylene, or paraffin did not independently compromise IHC performance in adequately fixed specimens.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149108957","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 of HSP72 in alleviating heat stress-induced damage in Sertoli cells of dairy bulls.","authors":"Haodi Zhang, Long Xie, Haoying Wang, Xueying Yan, Han Chen, Yingxue Wei, Zihan Geng, Shiyong Zhu, Zhongling Jiang, Huatao Li, Rongfeng Cao, Kaiqiang Fu","doi":"10.1007/s00418-026-02541-2","DOIUrl":"10.1007/s00418-026-02541-2","url":null,"abstract":"<p><p>Sertoli cells (SCs), the essential functional units of the testis, are responsible for supporting spermatogenesis. Heat stress impairs SCs by triggering oxidative injury, apoptosis, and ferroptosis, consequently suppressing spermatogenesis. Nevertheless, the dynamic alterations of SCs upon sustained heat stress remain poorly defined. Although HSP72 is recognized to exert a vital pro-survival function under heat stress, its detailed molecular mechanism remains largely elusive. The present study aimed to investigate the protective effect of HSP72 against heat stress-induced damage in SCs. Our results revealed that heat stress treatment for 1-6 h markedly suppressed cell viability, with a highly significant elevation in the apoptotic rate observed at the 6-h time point. Furthermore, either knockdown of Hsp72 or perturbation of the components of its functional complex markedly increased cellular susceptibility to heat stress, wherein a significant rise in apoptosis was detected as early as 1 h post heat exposure. We additionally evaluated the influence of heat stress on cell proliferation; prolonged heat stress for 6 h caused highly significant repression of cell proliferation, and Hsp72 knockdown resulted in pronounced proliferation inhibition regardless of heat stress exposure status. Further mechanistic assays demonstrated that HSP72 depletion dramatically upregulated P21 expression, leading to cell cycle arrest at the G₂ phase. Moreover, intracellular galactosidase activity was significantly elevated following 1-6 h of heat stress, and HSP72 silencing further increased the percentage of galactosidase-positive cells. Collectively, these findings highlight the crucial protective role of HSP72 in counteracting heat stress-elicited cellular injury, laying a fundamental theoretical foundation for alleviating heat-induced cellular damage.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069552","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":"<ArticleTitle xmlns:ns0=\"http://www.w3.org/1998/Math/MathML\">Proteomic study for the prediction of <ns0:math><ns0:mi>μ</ns0:mi></ns0:math> CT imaging with iodine.","authors":"Valentin Wesp, Heiko Stark, Lisa-Marie Barf","doi":"10.1007/s00418-026-02532-3","DOIUrl":"10.1007/s00418-026-02532-3","url":null,"abstract":"<p><p>Iodine-based staining techniques are commonly used in histological imaging and micro-computed tomography ( <math><mi>μ</mi></math> CT) because iodine binds to specific molecules. However, the basis for tissue-specific contrast has not yet been sufficiently explored. In this study, we analysed the human proteome at four levels: individual proteins, protein families, tissues with additional expression values for selected proteins, and organs as distinct combinations of tissues. At each level, we identified groups with high potential for iodine binding, particularly those rich in aromatic heterocyclic amino acids. We evaluated the occurrence of aromatic and non-aromatic heterocyclic and carbocyclic amino acids in 20,650 proteins, 1487 protein families, 57 tissues, and 16 organs using bioinformatic methods. This evaluation was based on curated human protein sequences and integrated expression information from the Human Protein Atlas and ProteomicsDB. At the protein level, structural proteins such as titin, nebulin, obscurin, mucin, filaggrin, and hornerin exhibited a high absolute number of aromatic heterocyclic amino acids, which could explain the high <math><mi>μ</mi></math> CT contrast in muscle, skin, and mucosal tissues. A smaller set of proteins displayed strong relative enrichment. At the family level, the average absolute values were highest in families containing very large proteins. However, relative values highlighted sequence-level enrichment in selected enzyme- and membrane-associated families. In contrast, tissue- and organ-level enrichment showed only small, non-significant differences depending on the expression dataset, and was highly similar across groups. Furthermore, enrichment was not robustly associated with iodine staining intensity in organs. Our results provide a foundation for iodine-based tissue imaging and could serve as a starting point for future research, such as cross-species applications and the structural and functional effects of iodination.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13615082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149060587","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":"Quercetin enhances the renoprotective effects of phosphodiesterase inhibitors by attenuating endoplasmic reticulum stress-induced cellular apoptosis via modulation of GRP75/CHOP/Bax/Bcl2 pathway.","authors":"Gehad Nasr, Doaa Mohamed Elroby Ali, Michael A Fawzy, Fares E M Ali, Moustafa Fathy","doi":"10.1007/s00418-026-02534-1","DOIUrl":"10.1007/s00418-026-02534-1","url":null,"abstract":"<p><p>This study investigated the ability of quercetin (QU) alone or with sildenafil (Sild) or pentoxifylline (PTX) to modulate carbon tetrachloride (CCl₄)-induced renal fibrosis in Wistar albino rats. Renal fibrosis was induced by intraperitoneal injection of CCl₄ (1.5 ml/kg, three times weekly for 10 weeks). Rats received oral doses of QU (50 mg/kg once daily), PTX (50 mg/kg once daily), and Sild (10 mg/kg twice daily) separately or in combination from week 7 to week 10. CCl₄ induced severe renal injury as indicated by urinary electrolytes disturbance, renal function impairment, increased oxidative stress, inflammation, up-regulation of endoplasmic reticulum (ER) stress markers (CHOP, GRP75), and apoptosis (Bax), as well as down-regulation of defense proteins (Bcl2, Nrf2, HO-1). QU, Sild, and PTX, alone or in combination, improved renal function and alleviated histological changes. The combination of QU with Sild or PTX resulted in greater renoprotection by regulating several key pathways, including reductions in ER stress, enhanced antioxidative defenses, and regulation of apoptosis. In conclusion, a combination of QU with Sild or PTX ameliorates renal fibrosis by inhibiting ER stress-induced cellular apoptosis through modulation of the GRP75/CHOP/Bax/Bcl2 and oxidative stress pathways.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149038278","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":"Lactational exposure to polystyrene nanoplastics induces oxidative stress, testicular histological alterations, and impaired sperm quality in rat offspring.","authors":"Saeid Fathollahi, Hamid Reza Moradi, Zabihollah Khaksar, Mohammad-Reza Divar, Sajjad Abbasi","doi":"10.1007/s00418-026-02539-w","DOIUrl":"10.1007/s00418-026-02539-w","url":null,"abstract":"<p><p>The widespread presence of nanoplastics in the environment has raised concerns regarding their potential adverse effects on reproductive health, particularly during the early developmental stages. Among these contaminants, polystyrene nanoplastics (PSNPs) can cross biological barriers and accumulate in tissues; however, the reproductive consequences of lactational exposure remain insufficiently understood. This study investigated the effects of maternal exposure to PSNPs during lactation on testicular development, oxidative stress, spermatogenesis, and sperm quality in male rat offspring on postnatal days (PD) 30 and 60. Lactating Sprague Dawley rats were orally administered PSNPs at doses of 0.1, 1, or 10 mg/kg/day from postnatal days 1 to 21. Male offspring were evaluated on PD30 and PD60. Testicular morphometry, histopathological alterations, oxidative stress biomarkers, reproductive hormone levels, sperm characteristics, and immunohistochemical expression of p53 and BCL-2 were also assessed. Histopathological examination revealed degeneration of seminiferous tubules, reduction in germinal epithelium height, and impaired spermatogenic organization, particularly at higher exposure doses. Significant alterations in oxidative stress biomarkers were observed, characterized by an increased total oxidant status and oxidative stress index, accompanied by a reduced antioxidant capacity. Sperm analysis revealed reductions in sperm count, motility, and viability, along with increased morphological abnormalities in the exposed groups. Hormonal evaluation indicated disturbances in serum testosterone, luteinizing hormone, and follicle-stimulating hormone (FSH) levels. Immunohistochemical analyses further demonstrated increased p53 expression and reduced BCL-2 immunoreactivity, suggesting the activation of apoptosis-related pathways. Lactational exposure to PSNPs adversely affects testicular development and sperm quality in male offspring, potentially through oxidative stress and apoptosis-related mechanisms. These findings suggest that early life exposure to nanoplastics during critical developmental periods may contribute to reproductive dysfunction, highlighting the need for further investigation into the long-term biological effects of environmental nanoplastic exposure.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149024756","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":"Dnmt3b and Dnmt3l knockdown reduces blastocyst development in early mouse embryos.","authors":"Nazlican Bozdemir, Ozgur Cinar, Tugce Oznacar, Ahmet Cevdet Ceylan, Fatma Uysal Cinar","doi":"10.1007/s00418-026-02540-3","DOIUrl":"10.1007/s00418-026-02540-3","url":null,"abstract":"<p><p>A one-cell embryo called a zygote develops into a blastocyst through several successive cell divisions and lineage specification, this process is called early embryo development. Both embryonic genome activation (EGA) and the first lineage specification during early embryonic development depend on tightly coordinated epigenomic organization. Regulation of the epigenome is primarily governed by DNA methylation mediated through DNA methyltransferase (Dnmt) enzymes. Dnmt1 is responsible for the maintenance of methylation during cellular division, while Dnmt3a/Dnmt3b enzymes play a role in the establishment of de novo methylation particularly during gametogenesis and early embryo development. Despite its lack of catalytic activity, Dnmt3l functions as a cofactor enhancing Dnmt3a/3b activity. Dnmt3b deficiency results in global hypomethylation and ultimately embryonic lethality. In this study, we aim to elucidate the effect of Dnmt3b and Dnmt3l silencing on early embryo development. For this purpose, our experimental groups were established using an in vitro mouse embryo development model: control, Dnmt3b small interfering RNA (siRNA), Dnmt3l siRNA, and a nontargeting siRNA group. Following gene silencing at the one-cell stage, embryonic developmental competence, the expression pattern of nonsilenced Dnmt enzymes, global DNA methylation levels, and transcriptome profiles were analyzed at the blastocyst stage. Dnmt3b/3l silencing resulted in decreased global DNA methylation and Dnmt1/3a expression, and reduced blastocyst rate. Differentially expressed genes included those involved in X-chromosome inactivation (Xist), transcriptional regulation (Rn7sk), translation (Eef1a1, Eef2), trophoblast development (Hsd3b1), compaction (Gja1), and oxidative phosphorylation (CYTB, COX1, mt-Rnr1). Our findings indicate that siRNA-mediated knockdown of Dnmt3b and Dnmt3l is associated with reduced blastocyst development, impaired embryo quality, and alterations in DNA methylation-related processes during early embryonic development.</p>","PeriodicalId":13107,"journal":{"name":"Histochemistry and Cell Biology","volume":"164 1","pages":""},"PeriodicalIF":2.9,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982620","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}