Molecular and Cellular Biochemistry最新文献

{"title":"Piezo1: the Potential Novel Target for Radiation-induced Liver Fibrosis by Regulating FAP + fibroblasts.","authors":"Wentong Liu, Haochen Zou, Jiaying Wei, Lihua Dong, Wei Hou","doi":"10.1007/s11010-025-05327-7","DOIUrl":"10.1007/s11010-025-05327-7","url":null,"abstract":"<p><p>Radiation-induced liver fibrosis is a serious complication of radiotherapy in patients with liver cancer and is characterized by excessive deposition of the extracellular matrix (ECM). The activation of cancer-associated fibroblasts (CAFs) is central to this event. Piezo1 is a mechanoreceptor that is highly expressed in liver tissue and is closely related to the fibrotic process. CAFs are highly heterogeneous, and different cell populations perform different functions. Recent studies have shown that fap, an important surface marker of the CAF membrane, presumably plays a \"hub\" role upstream of α-smooth muscle actin (α-SMA). This article reviews the unique microenvironment of liver cancer and liver fibrosis and the role of piezo1 and CAFs in liver fibrosis. Building upon the foundational evidence, we formulate a hypothesis that radiation-induced ECM remodeling activates Piezo1-mediated mechanotransduction, driving HIF-1α/TGF-β pathways to stimulate CAF activation (manifested by FAP upregulation), which may synergistically aggravate liver fibrosis and hepatocarcinogenesis.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5297-5308"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12515122/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144317478","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":"High IGFL2 regulates ovarian cancer progression and the tumor immune microenvironment via the Warburg effect.","authors":"Zhizai Chen, Dalong Song, Shuting Huang, Jinyu Chao, Junhong Huang, Ming Luo, Shanyang He","doi":"10.1007/s11010-025-05328-6","DOIUrl":"10.1007/s11010-025-05328-6","url":null,"abstract":"<p><p>This study aimed to explore the role and mechanism of insulin-like growth factor-like family member 2 (IGFL2) in ovarian cancer (OC) metastasis. Specifically, we focused on how IGFL2 regulates tumor cell energy metabolism and influences macrophage polarization to promote ovarian cancer metastasis. By conducting in vitro and in vivo experiments to elucidate the biological functions of IGFL2, this study aiming to identify new therapeutic targets for ovarian cancer treatment and provide a more effective treatment strategy. Our study revealed that the expression of IGFL2 was substantially upregulated in ovarian cancer metastases, and its high expression was positively correlated with the malignancy and metastatic potential of ovarian cancer. IGFL2 knockdown promoted mitochondrial oxidative phosphorylation and inhibited the Warburg effect, evidenced by increased oxygen consumption rate (OCR) and ATP production, and decreased glycolytic enzyme expression and lactate secretion. Concurrently, IGFL2 promoted M2 macrophage polarization via the STAT1/STAT6 signaling pathway, increasing the proportion of CD11b + CD206 + M2 cells and suppressing M1 polarization. In vivo, IGFL2 knockdown significantly inhibited tumor growth and metabolic reprogramming in xenograft models.These findings demonstrate that IGFL2 promotes OC metastasis through a dual mechanism: regulating metabolic reprogramming (Warburg effect) and influencing tumor-associated macrophage (TAM) polarization.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5485-5500"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Novel frequenin-modulated Ca2⁺-signaling membrane guanylate cyclase (ROS-GC) transduction pathway in bovine hippocampus.","authors":"Ewa Fik-Rymarkiewicz, Teresa Duda, Rameshwar K Sharma","doi":"10.1007/s11010-025-05381-1","DOIUrl":"10.1007/s11010-025-05381-1","url":null,"abstract":"","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5553"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000951","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Canagliflozin improves high-salt-induced aortic arteriosclerosis and premature aging in dahl salt-sensitive rats through the SIRT6/HIF-1 α signaling pathway.","authors":"Qiuyan Wang, Yi Liang, Qingjuan Zuo, Lili He, Tingting Zhang, Zhongli Wang, Jianlong Zhai, Boce Cao, Sai Ma, Guorui Zhang, Fan Lu, Kaichuan He, Yan Wang, Yifang Guo","doi":"10.1007/s11010-025-05321-z","DOIUrl":"10.1007/s11010-025-05321-z","url":null,"abstract":"<p><p>Hypertension and its complications seriously affect human health, bringing about long-term medical burdens, functional impairments and even death. This study explored the impact of Canagliflozin (CANA) on the blood vessels of salt-sensitive hypertension. Male Dahl salt-sensitive (Dahl SS) rats were fed with an 8% high-salt diet, and then intragastrically given CANA at a dose of 30 mg/kg/day or with a 0.5% hydroxypropyl methylcellulose solution for 12 weeks to induce hypertensive vascular damage and premature aging. Through vascular ultrasound detection, CANA improved the aortic stiffness and hemodynamics of high-salt-fed rats. Through vascular reactivity tests, CANA improved the carotid artery vasodilation. Hematoxylin and eosin (H&E), Sirius red, and senescence associated β-galactosidase staining were performed on the aorta, and CANA improved the fibrosis and aging of the aorta. CANA was found to reduce the expression of senescence associated secretory phenotype in the circulation that was induced by a high-salt diet. Additionally, it increased the expression of Sirtuin 6(SIRT6) in blood vessels and decreased the expression of Hypoxia-inducible factor 1α (HIF-1α) and its target genes. This study has demonstrated for the first time that CANA mitigates salt-induced aortic sclerosis and premature aging via the SIRT6/HIF-1α pathway.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5369-5385"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144199620","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Lacticaseibacillus rhamnosus LB1.5 as potential probiotic supplement on the liver and adipose tissue of adult male mice to a high-fat diet.","authors":"Natália Perin Schmidt, Milena Henrique Ferri, Patrícia Molz, Brenda Santos Fraga, Priscila Dutra Silveira, Daiana Rodrigues Dos Santos, Juan Andres Cuadro Montanez, Gabriela Merker Breyer, Amanda de Souza da Motta, Marilene Porawski, Alethea Gatto Barschak, Renata Padilha Guedes, Márcia Giovenardi","doi":"10.1007/s11010-025-05344-6","DOIUrl":"10.1007/s11010-025-05344-6","url":null,"abstract":"<p><p>This study aimed to investigate the effects of Lacticaseibacillus rhamnosus LB1.5 supplementation on liver and adipose tissue morphology, oxidative stress, and the relative gene expression of Sirt1, Gpx1, and Il6 in the liver of HFD-fed mice. Male C57BL/6 mice received: (i) a control diet (CONT), (ii) a control diet with probiotics (Lact. rhamnosus LB1.5, 1.3 × 10⁸ CFU/mL, three times a week; CONT + PROB), (iii) a high-fat diet (HFD), or (iv) a high-fat diet with probiotics (HFD + PROB) for 13 weeks. The HFD group showed significant liver alterations, including lipid accumulation, severe steatosis, hepatocellular ballooning, and an increase in Il6 relative gene expression, as well as an interaction effect on Sirt1 relative gene expression (p < 0.05). Nevertheless, these changes were not mitigated by probiotic supplementation (p > 0.05). Additionally, HFD-fed mice exhibited significant alterations in adipose tissue (p < 0.05), such as increased tissue weight, a lower number of adipocytes per area, and larger adipocyte size per area, with no significant effect of the probiotic observed (p > 0.05). In the liver, high TBARS levels were found in the HFD group, and a probiotic supplementation effect on sulfhydryl levels was observed only in the HFD + PROB group (p < 0.05). Unlike, in adipose tissue, redox status was not affected by diet or supplementation (p > 0.05). In conclusion, our results demonstrated the pro-inflammatory effects of an obesogenic diet and suggest that Lact. rhamnosus LB1.5 supplementation contributes only to the enhancement of liver redox status, improving antioxidant defenses by increasing sulfhydryl levels.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5531-5543"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528916","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of lncRNA-ZFAS1 in liver fibrosis: insights into the miR-1953/TAZ axis.","authors":"Binbo Fang, Weizhi Zhang, Mengyuan Li, Jianjian Zheng, Hui Jin","doi":"10.1007/s11010-025-05335-7","DOIUrl":"10.1007/s11010-025-05335-7","url":null,"abstract":"<p><p>Long non-coding RNA-Zinc finger antisense 1 (lncRNA-ZFAS1) is involved in the progression of several cancer types, yet its function in liver fibrosis remains unclear. The purpose of this study was to examine ZFAS1 expression in liver fibrosis and explore its possible molecular mechanism. ZFAS1 expression was measured in a liver fibrosis model and in activated hepatic stellate cells (HSCs). The impact of ZFAS1 silencing on HSC growth, collagen production, and epithelial-mesenchymal transition (EMT) was assessed. The connection between ZFAS1 and miR-1953 was investigated using bioinformatics analysis and luciferase reporter gene experiments. Moreover, in vivo studies were performed to confirm the effect of ZFAS1 knockdown on liver fibrosis progression. ZFAS1 was significantly upregulated in the liver fibrosis model and activated HSCs. Silencing ZFAS1 helped to inhibit the growth and activation of HSCs, along with reduced levels of type I collagen and α-SMA. In vivo experiments confirmed that ZFAS1 knockdown alleviated the progression of fibrosis and collagen deposition. Mechanistic studies revealed that ZFAS1 promoted HSC EMT through the regulation of the miR-1953/TAZ axis, thereby exerting a pro-fibrotic effect. By influencing the miR-1953/TAZ signaling pathway, ZFAS1 significantly contributes to the activation and EMT of HSCs in liver fibrosis development. These findings highlight ZFAS1 as a potential therapeutic target for treating liver fibrosis, offering new avenues for clinical intervention.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5473-5484"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144317479","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treatment with crocin attenuates cardiac metabolic disturbances and subsequent inflammation in streptozotocin-induced diabetes.","authors":"Dimitra Palioura, Konstantinos Feidantsis, Antigone Lazou","doi":"10.1007/s11010-025-05320-0","DOIUrl":"10.1007/s11010-025-05320-0","url":null,"abstract":"<p><p>Diabetes mellitus (DM) is a metabolic disorder closely associated with cardiac dysfunction. Natural products are considered potential candidates for the management of DM. Crocin, a natural carotenoid derived from saffron, has been reported to possess several pharmacological properties, including cardioprotective effects. The aim of the present study was to investigate the beneficial effects of crocin on the metabolic derangement of the diabetic myocardium. Streptozotocin (STZ)-induced diabetic rats were treated with 10 mg/kg of crocin daily for two weeks. Oral administration of crocin normalized blood glucose, HbA1c, triglycerides, total cholesterol, LDL, and HDL levels. Notably, crocin reduced the elevated protein levels of cardiac PPARα and PPARδ-major transcriptional regulators of cardiac metabolism-back to normal. Consequently, the expression of the fatty acid (FA) transporter CD36 was downregulated, the activity of the FA oxidation enzyme 3-hydroxyacyl-CoA dehydrogenase (HOAD) was decreased, and intramyocardial triglyceride accumulation returned to physiological levels. Furthermore, crocin improved glucose uptake and metabolism in the diabetic myocardium, as evidenced by increased Akt phosphorylation, translocation of GLUT4 to the plasma membrane, enhanced activity of pyruvate kinase, and downregulation of pyruvate dehydrogenase kinase 4 (PDK4). Importantly, the stimulatory effect of crocin on Akt phosphorylation was also confirmed in isolated cardiac myocytes exposed to high glucose, further supporting its direct role in modulating glucose signaling pathways. Crocin treatment also reduced STZ-induced elevations in the levels of inflammatory cytokines-interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)-as well as the phosphorylation of IκBα, bringing them close to basal levels. Overall, these findings suggest that crocin activates Akt signaling and thereby alleviates diabetes-induced metabolic disturbances by restoring the balance between glucose and fatty acid utilization in the hearts of STZ-induced diabetic rats. Therefore, crocin supplementation may represent a promising approach for the development of natural compound-based adjunct therapies for diabetic cardiomyopathy.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":"5387-5397"},"PeriodicalIF":3.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12515198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144216346","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":"Interconnection between gut microbial metabolites and mitochondrial ROS production: implications for cellular health.","authors":"Priyanka Gupta, Sumit Dutta, Krishanu Dutta, Piyush Bhattacharjee, Arjama Hazra, Rajiv Jash","doi":"10.1007/s11010-025-05397-7","DOIUrl":"https://doi.org/10.1007/s11010-025-05397-7","url":null,"abstract":"<p><p>Trillions of microbes inhabit the human gut and engage in diverse biological processes by secreting different metabolites. These metabolites influence mitochondrial function and produce ROS. This gut-mitochondrial communication plays a pivotal role in regulating cellular homeostasis, energy production, and oxidative stress management, all required for optimal health. Short-chain fatty acids, secondary bile acids, amines, and gaseous metabolites are major gut metabolites that aid in governing mitochondrial processes to facilitate effective energy production and avoid oxidative damage. In the case of damaged mitochondrial function, it can alter gut flora (dysbiosis), resulting in inflammation and assisting a number of diseases such as multiple sclerosis, Alzheimer's disease, IgA nephropathy, inflammatory bowel disease, and colorectal cancer. The gut-mitochondria axis is a multifaceted interaction that regulates a cell's energy homeostasis and provides novel therapeutic opportunities. Probiotics, prebiotics, dietary modifications, and metabolite therapies have the potential to restore gut-microbe balance, enhance mitochondrial function, and reduce oxidative stress. These measures have the potential for new treatments for many diseases by modulating the gut-mitochondria axis. This review surveys interactions among gut microbiota, mitochondrial ROS, and the gut-mitochondria axis, describing how such relationships affect health and disease.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145200374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Monoamine oxidases are mediators of oxidative stress in human varicose Veins: interactions with obesity, inflammation, and angiotensin II.","authors":"Sonia Raţiu, Adrian Sturza, Paul S Muntean, Claudia Borza, Tiberiu Bratu, Danina M Muntean","doi":"10.1007/s11010-025-05398-6","DOIUrl":"https://doi.org/10.1007/s11010-025-05398-6","url":null,"abstract":"<p><p>Chronic venous disease (CVD) and its clinical manifestation, the varicose veins (VVs), are characterized by progressive structural and functional alterations of the venous walls, with obesity/overweight being one of the most frequent comorbidities. Monoamine oxidases (MAO-A and MAO-B) are mitochondrial flavoenzymes responsible for the constant generation of hydrogen peroxide (H₂O₂) during the catabolism of biogenic monoamines and neurotransmitters that contribute, when upregulated, to the oxidative stress in most mammalian tissues. However, their role in the VV pathophysiology and its modulation by vasoactive stimuli such as angiotensin II (Ang II) remains unclear. This exploratory study was double-aimed i) to assess MAO expression in human VV samples in relation to obesity and systemic inflammation and ii) to determine the impact of pharmacological MAO inhibition on oxidative stress under basal and Ang II-stimulated conditions. To this aim, 20 patients with VV and an indication for cryostripping were randomized according to their body mass index (BMI) into obese (n = 10) and non-obese (n = 10) groups, and VV samples were harvested and used to assess the following: i) MAO-A and MAO-B gene expression by qRT-PCR, as well as expression and localization by immunofluorescence, and ii) H₂O₂ by means of the ferrous xylenol orange oxidation (FOX) assay. Furthermore, the effect of selective MAO inhibition (clorgyline 10 μM for MAO-A, selegiline 10 μM for MAO-B) was tested ex vivo both at baseline and following acute stimulation with Ang II (100 nM). We showed that both MAO-A and MAO-B are constitutively expressed in the human venous walls, with higher levels in the varicose veins than in the adjacent perforator veins. The obese patients with inflammatory status (elevated serum C-reactive protein) had significantly increased MAO-A (but not MAO-B) expression as compared to the non-obese controls (p < 0.01). Acute ex vivo incubation with Ang II further enhanced the expression of both isoforms and increased H₂O₂ generation. MAO inhibition significantly mitigated the oxidative stress in both non-stimulated and Ang II-stimulated samples, regardless of the presence or absence of obesity. In conclusion, MAO isoforms, in particular MAO-A, are upregulated in the human varicose veins and can be further induced by Ang II, especially in the setting of obesity associated with low-grade inflammation. MAO contributed to the local oxidative stress, which was significantly reduced by its pharmacological inhibition with MAO-A and B inhibitors, thus pointing to MAO as a potential therapeutic target in patients with CVD.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145186373","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FKH domain-mediated nuclear FOXP3 suppresses gastric cancer malignancy via c-MYC/CDKN1A regulation, EMT inhibition, and PI3K/AKT signaling modulation.","authors":"Yu Chen, Xia Zhao, Yuze Zhu, Ling Xu, Juanjuan Wang, Zheyi Chen, Hui Chen, Tingting Rong, Yanhui Ma, Yi Liu, Yunlan Zhou, Yingxia Zheng, Lisong Shen, Guohua Xie","doi":"10.1007/s11010-025-05387-9","DOIUrl":"https://doi.org/10.1007/s11010-025-05387-9","url":null,"abstract":"<p><p>Gastric cancer (GC) remains a primary contributor to cancer-associated deaths worldwide, especially in East Asia. We investigated the function of nuclear-localized full-length FOXP3 (FOXP3FL) as an oncosuppressive factor in GC. Total FOXP3 was markedly reduced in GC tissues versus adjacent normal mucosa, with distinct cytoplasmic and nuclear patterns. Functional assays revealed that nuclear overexpression of FOXP3FL suppresses proliferation, migration, and invasion of GC cells in vitro and in vivo and promotes cellular senescence in vivo. Mechanistically, FOXP3FL directly represses MYC transcription and induces CDKN1A, thereby restraining proliferation and metastasis. These transcriptional changes, together with concomitant PTEN upregulation and PI3K-P110α downregulation, collectively attenuate PI3K/AKT signaling and impair epithelial-mesenchymal transition (EMT) in FOXP3FL-expressing GC cells. The forkhead (FKH) domain is essential: its deletion yields cytoplasmic FOXP3ΔFKH, which loses transcriptional control and antitumor activity. Our findings underscore nuclear-localized FOXP3FL as a tumor suppressor whose FKH domain is integral to its suppressive function.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145137999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}