Cells最新文献

{"title":"Extracellular Vesicles (EVs) Derived from Mesenchymal Stem Cells (MSCs) as Adjuvants in the Treatment of Chronic Kidney Disease (CKD).","authors":"Paloma Noda, Ana L R Francini, Flavio Teles, Samuel J Júnior, Fernando L A Fonseca, Fernanda T Borges, Adão C Sobrinho, Noemi Taniwaki, Irene L Noronha, Camilla Fanelli","doi":"10.3390/cells14060434","DOIUrl":"10.3390/cells14060434","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) is considered an important health issue worldwide. The renin-angiotensin-aldosterone system (RAAS) blockade through the administration of angiotensin II receptor blockers, such as Losartan (LOS), has been considered the best strategy for CKD treatment for decades. However, this approach promotes only partial detention of CKD progression and cannot reverse renal damage. The aim of the present study was to investigate whether the therapeutic administration of extracellular vesicles (EVs) derived from adipose stem cells (ASCs), associated to LOS treatment, would promote additional renoprotection in rats underwent the 5/6 renal ablation CKD model. ASC-derived EV were administered locally, in the renal subcapsular area, 15 days after CKD induction, when LOS therapy also began. Animals were followed for additional 15 days and our results demonstrated that subcapsular injection of ASC-derived EV associated with LOS significantly reduced glomerulosclerosis, renal interstitial infiltration by myofibroblasts, and macrophages in the 5/6 CKD model. Additionally, LOS + EV abrogated systemic hypertension, proteinuria, and albuminuria, and stimulated local gene overexpression of the endogenous anti-inflammatory <i>Il-4</i>. Although more studies are still required to establish the best EV dose and administration route, these findings point to therapy with ASC-derived EV as a potential adjuvant in CKD treatment.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 6","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Hypoxia-Inducible Factor-1α (HIF-1α) in the Progression of Ovarian Cancer: Perspectives on Female Infertility.","authors":"Md Ataur Rahman, Maroua Jalouli, Sujay Kumar Bhajan, Mohammed Al-Zharani, Abdel Halim Harrath","doi":"10.3390/cells14060437","DOIUrl":"10.3390/cells14060437","url":null,"abstract":"<p><p>Hypoxia-Inducible Factor-1α (HIF-1α) is crucial in the progression of ovarian cancer, especially in influencing its tumor microenvironment and promoting pathogenic pathways that worsen female infertility. In hypoxic settings, HIF-1α is stabilized and activates the transcription of genes associated with angiogenesis, metabolic reprogramming, epithelial-to-mesenchymal transition, and therapeutic resistance. Angiogenesis and glycolytic reprogramming mediated by HIF-1 tumor proliferation, survival, and metastasis. Its dysfunction concurrently impairs ovarian homeostasis, undermining follicular growth, hormone synthesis, and the ovarian vascular network, consequently contributing to infertility. Moreover, HIF-1α induces persistent inflammation and oxidative stress, promoting an environment damaging to reproductive health. Due to its dual function in ovarian cancer growth and infertility, HIF-1α is a potential therapeutic target. Strategies including small molecule inhibitors and nanoparticle-mediated delivery of drugs possess the potential to reduce HIF-1α activity, hence reducing cancer progression while protecting fertility. This review seeks to clarify the molecular basis of HIF-1α in ovarian cancer and its effects on female infertility, providing insights into novel treatment approaches that target both controlling the disease and preserving fertility.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 6","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lysine Demethylase 1 Has Demethylase-Dependent and Non-Canonical Functions in Myofibroblast Activation in Systemic Sclerosis.","authors":"Christopher W Wasson, Esther Perez Barreiro, Francesco Del Galdo, Natalia A Riobo-Del Galdo","doi":"10.3390/cells14060433","DOIUrl":"10.3390/cells14060433","url":null,"abstract":"<p><p>Systemic sclerosis (SSc) is an autoimmune disease of unknown aetiology characterised by vasculopathy with progressive fibrosis of the skin and internal organs. Tissue fibrosis is driven by activated fibroblasts (myofibroblasts) with exacerbated contractile and secretory properties. We previously reported that the long non-coding RNA HOTAIR is a key driver of SSc fibroblast activation. HOTAIR interacts with the chromatin modifiers, the polycomb repressor complex (PRC2) and coREST complex, promoting expression of pro-fibrotic genes. In this study, we show that acute activation of dermal fibroblasts from healthy subjects or SSc patients with transforming growth factor-β and other fibrotic stimuli requires the activity of the lysine-specific demethylase 1 (LSD1) subunit of the co-REST complex. Unexpectedly, LSD1 catalytic activity plays a minor role in fibrotic gene expression in HOTAIR-overexpressing fibroblasts and in maintenance of the stable myofibroblast phenotype of SSc fibroblasts. However, silencing of LSD1 in SSc fibroblasts has a profound effect on pro-fibrotic gene expression, supporting a non-canonical scaffolding function. Our study shows for the first time an essential non-canonical role for LSD1 in pro-fibrotic gene expression in SSc; however, given that this function is insensitive to LSD1 inhibitors, the therapeutic opportunities will depend on future identification of a targetable mediator.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 6","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SR-FTIR Biomolecular Characterization of the Hippocampus: The Role of Tenascin C in Adult Murine Neurogenesis in the Subgranular Zone.","authors":"Milena Korenić, Andrej Korenić, Vera Stamenković, Tanja Dučić, Pavle Andjus","doi":"10.3390/cells14060435","DOIUrl":"10.3390/cells14060435","url":null,"abstract":"<p><p>To better understand adult neurogenesis, the biomolecular specificity of the subgranular zone should be investigated in comparison to other layers of the hippocampus. Adult neurogenesis occurs at a reduced rate in adulthood compared to the period of development, but it can be increased with exposure to an enriched environment (EE). This can be used to investigate the regulatory role of molecules present in the extracellular matrix, such as tenascin C (TnC). This study, using Synchrotron radiation Fourier Transform Infrared spectroscopy (SR-FTIR), shows that the differences between the hippocampal layers in adolescence are maintained as subtle and significant in adulthood. The main difference in FTIR spectra was observed for nucleic acid and carbohydrate and for the comparison of the subgranular zone (SGZ) with hippocampal CA3. Moreover, we have detected changes in the protein and nucleic acid content of the SGZ that accompany the process of neurogenesis under the influence of an enriched environment. The latter effects are, however, lacking in mice with a gene ablation for tenascin C. Overall, these results show that observed discrete biomolecular differences in hippocampal layers follow the rate of neurogenesis that is enhanced by EE and dependent on TnC.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 6","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941197/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Long-Term Regulation of IL-17 Expression in Pacific Oyster Hemocytes by mGluR5 Through the Phosphoinositide Pathway.","authors":"Yiran Si, Deliang Li, Wenjing Ren, Xueshu Zhang, Lingling Wang, Linsheng Song","doi":"10.3390/cells14060438","DOIUrl":"10.3390/cells14060438","url":null,"abstract":"<p><p>Metabotropic glutamate receptor 5 (mGluR5) is a critical regulator of immune responses within the neuroimmune system, influencing cytokine secretion and immune cell function. Although extensively studied in mammals, its role in regulating IL-17 in invertebrate immunity is poorly understood. This study examines <i>CgmGluR5</i> expression and downstream signaling activation in Pacific oyster (<i>Crassostrea gigas</i>) hemocytes following glutamate (Glu) and <i>Vibrio splendidus</i> treatment. Glu treatment significantly induced the expression of <i>CgmGluR5</i> and key signaling molecules, including PLC, DAG, IP3, Ca²⁺, and PKC, while enhancing mRNA levels of <i>CgIL17-1</i>, <i>CgIL17-5</i>, and <i>CgCaspase3</i>. Elevated Ca²⁺ content and <i>CgIL17</i> expression in hemocytes were observed at 12 h post-Glu exposure, indicating <i>CgmGluR5</i>-mediated immune regulation through the phosphoinositide pathway. A 1.14-fold increase in the apoptosis rate was found in the Glu treatment group compared to the control group. Knockdown of <i>CgmGluR5</i> suppressed <i>CgIL17-1</i> and <i>CgIL17-5</i> expression and reduced granulocyte proportions, reflecting its role in immune regulation. This study shows that <i>CgmGluR5</i> mediates long-term immune regulation in oysters through the phosphoinositide pathway, providing new theoretical insights for aquaculture immune management.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 6","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941601/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blockade of HSP70 Improves Vascular Function in a Mouse Model of Type 2 Diabetes.","authors":"Valentina Ochoa Mendoza, Amanda Almeida de Oliveira, Kenia Pedrosa Nunes","doi":"10.3390/cells14060424","DOIUrl":"10.3390/cells14060424","url":null,"abstract":"<p><p>Type 2 diabetes (T2D) is a chronic disease that damages blood vessels and increases the risk of cardiovascular disease (CVD). Heat-shock protein 70 (HSP70), a family of chaperone proteins, has been recently reported as a key player in vascular reactivity that affects large blood vessels like the aorta. Hyperglycemia, a hallmark of diabetes, correlates with the severity of vascular damage and circulating HSP70 levels. In diabetes, blood vessels often show impaired contractility, contributing to vascular dysfunction. However, HSP70's specific role in T2D-related vascular contraction remains unclear. We hypothesized that blocking HSP70 would improve vascular function in a widely used diabetic mouse model (db/db). To test this, we measured both vascular intracellular and serum circulating HSP70 levels in control and diabetic male mice using immunofluorescence and Western blotting. We also examined the aorta's contractile response using a wire myograph system, which measured the force produced in response to phenylephrine (PE), both with and without VER155008, a pharmacological inhibitor that targets the ATPase domain of HSP70, and after removing extracellular calcium. Our findings show that intracellular HSP70 (iHSP70) levels were similar in control and diabetic groups, while circulating HSP70 (eHSP70) levels were higher in the serum of diabetic mice, altering the iHSP70/eHSP70 ratio. Even though VER155008 attenuated both phases of the contractile curve in the diabetic and control groups, enhanced vasoconstriction to PE was only observed in the tonic phase of the curve in the db/db group, which was prevented by iHSP70 inhibition. This effect involved calcium mobilization, as both the maximal and total contraction forces to PE were restored in groups treated with VER155008. Additionally, internal calcium levels in aortic rings treated with VER155008 decreased, as observed in force generation upon calcium reintroduction, which was further corroborated using a biochemical calcium assay. In conclusion, our study demonstrates that blocking HSP70 improves vascular reactivity in the hyperglycemic state of T2D by restoring proper vascular contraction.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 6","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941590/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathogenic Mechanisms of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD)-Associated Hepatocellular Carcinoma.","authors":"Toru Nakamura, Atsutaka Masuda, Dan Nakano, Keisuke Amano, Tomoya Sano, Masahito Nakano, Takumi Kawaguchi","doi":"10.3390/cells14060428","DOIUrl":"10.3390/cells14060428","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is the sixth most common cancer and the third leading cause of cancer deaths worldwide. The etiology of HCC has now dramatically changed from viral hepatitis to metabolic dysfunction-associated steatotic liver disease (MASLD). The main pathogenesis of MASLD-related HCC is the hepatic lipid accumulation of hepatocytes, which causes chronic inflammation and the subsequent progression of hepatic fibrosis. Chronic hepatic inflammation generates oxidative stress and DNA damage in hepatocytes, which contribute to genomic instability, resulting in the development of HCC. Several metabolic and molecular pathways are also linked to chronic inflammation and HCC in MASLD. In particular, the MAPK and PI3K-Akt-mTOR pathways are upregulated in MASLD, promoting the survival and proliferation of HCC cells. In addition, MASLD has been reported to enhance the development of HCC in patients with chronic viral hepatitis infection. Although there is no approved medication for MASLD besides resmetirom in the USA, there are some preventive strategies for the onset and progression of HCC. Sodium-glucose cotransporter-2 (SGLT2) inhibitor, a class of medications, has been reported to exert anti-tumor effects on HCC by regulating metabolic reprogramming. Moreover, CD34-positive cell transplantation improves hepatic fibrosis by promoting intrahepatic angiogenesis and supplying various growth factors. Furthermore, exercise improves MASLD through an increase in energy consumption as well as changes in chemokines and myokines. In this review, we summarize the recent progress made in the pathogenic mechanisms of MASLD-associated HCC. Furthermore, we introduced new therapeutic strategies for preventing the development of HCC based on the pathogenesis of MASLD.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 6","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941585/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708774","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In Vitro Exposure to the Endocrine-Disrupting Chemical Climbazole Impairs Human Sperm Motility, Hormonal Signalling, and Mitochondrial Activity.","authors":"Eugenia Annunzi, Francesca Paola Luongo, Francesca Girolamo, Rosetta Ponchia, Sofia Passaponti, Paola Piomboni, Alice Luddi","doi":"10.3390/cells14060427","DOIUrl":"10.3390/cells14060427","url":null,"abstract":"<p><p>This study explores the endocrine-disrupting effects of climbazole (CBZ), an environmental and lifestyle stressor, on male fertility. The impact of CBZ on sperm vitality, motility, and molecular pathways related to hormone receptors and apoptosis was evaluated, in non-capacitated and capacitated conditions. Gene expression of key components, including hormone receptors (<i>ESR1</i>, <i>ESR2</i>, <i>FSHR</i>, <i>AR</i>), apoptosis-related genes (<i>BAX</i>, <i>BCL2</i>), and <i>COX4l1</i> (involved in mitochondrial function), was analyzed. Protein tyrosine phosphorylation, a marker of capacitation, was also examined using immunofluorescence and Western blot analysis. We demonstrated that CBZ significantly reduced sperm vitality at concentrations above 25 µM and motility at 1 and 10 µM in non-capacitated and capacitated conditions. Changes in tyrosine phosphorylation patterns were also observed. Gene expression analysis revealed an upregulation of <i>ESR1</i>, <i>ESR2</i>, <i>FSHR</i>, and <i>BAX</i>, while <i>AR</i> and <i>COX4l1</i> expression were downregulated. These findings offer new insights into the potential endocrine-disrupting and cytotoxic effects of CBZ, highlighting its potential role in compromising male reproductive health.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 6","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11940937/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammatory Modulation of Toll-like Receptors in Periodontal Ligament Stem Cells: Implications for Periodontal Therapy.","authors":"Mohamed Mekhemar, Immo Terheyden, Christof Dörfer, Karim Fawzy El-Sayed","doi":"10.3390/cells14060432","DOIUrl":"10.3390/cells14060432","url":null,"abstract":"<p><p>Toll-like receptors (TLRs) play a crucial role in the innate immune response, mediating cellular interactions with the microenvironment and influencing periodontal disease progression. This in vitro study aimed to comprehensively characterize the TLR expression profile of periodontal ligament mesenchymal stem/progenitor cells (PDLSCs) and investigate its modulation by inflammatory stimuli associated with periodontal disease. PDLSCs (<i>n</i> = 6) were isolated, selected using anti-STRO-1 antibodies, and cultured to evaluate their colony-forming abilities and stem/progenitor characteristics. Baseline and inflammation-induced TLR expressions were evaluated using RT-PCR and protein analyses following cytokine-mediated stimulation. PDLSCs exhibited the expected stem cell characteristics and expressed multiple TLRs under both conditions. Notably, inflammatory stimulation significantly upregulated TLR1 and TLR2 while downregulating TLR10 (<i>p</i> < 0.05). These findings provide a comprehensive characterization of TLR expression in PDLSCs and demonstrate how inflammation modulates their innate immune profile. The observed shifts in TLR expression may influence PDLSC responses to microbial pathogens and impact their immunomodulatory and regenerative properties in periodontal tissues. Understanding these interactions could contribute to developing targeted strategies for improving PDLSC-based therapies in periodontal disease.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 6","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11941712/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708732","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lateral Ventricular Neural Stem Cells Provide Negative Feedback to Circuit Activation Through GABAergic Signaling.","authors":"Moawiah M Naffaa, Henry H Yin","doi":"10.3390/cells14060426","DOIUrl":"10.3390/cells14060426","url":null,"abstract":"<p><p>Recent studies have demonstrated that circuit activation in vivo can regulate proliferation of lateral ventricular neural stem cells (LV NSCs), although the underlying molecular and cellular mechanisms are not yet fully understood. Here, we investigated the role of GABAergic signaling in the interaction between LV NSCs and the anterior cingulate cortex-subependymal-choline acetyltransferase⁺ (ChAT⁺) neuron (ACC-subep-ChAT⁺) circuit. We found that monoamine oxidase B (MAOB), a key enzyme involved in gamma-aminobutyric acid (GABA) synthesis, is expressed in LV NSCs, and that activation of the ACC-subep-ChAT⁺ circuit can modulate MAOB activity. Additionally, LV NSCs express LRRC8D, a core component of volume-regulated anion channels, and GABA transporter-1 (GAT-1, SLC6A1). We show evidence that, through GABA signaling, LRRC8D and GAT-1 can provide a negative feedback signal to ChAT⁺ neurons, a key component of the ACC-subep-ChAT⁺ circuit that regulate proliferation of LV NSCs. These findings suggest that MAOB-driven GABA synthesis, LRRC8D-regulated chloride and GABA transport, and GAT-1-facilitated GABA reuptake can regulate neural circuit activation and influence NSC proliferation dynamics in the LV.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 6","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11940892/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}