Molecular and Cellular Biochemistry最新文献_第3页

The role of ACSL4 in stroke: mechanisms and potential therapeutic target. ACSL4 在中风中的作用：机制和潜在治疗目标。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2024-11-04 DOI: 10.1007/s11010-024-05150-6

Bifang Zhuo, Chenyang Qin, Shizhe Deng, Hailun Jiang, Shangkun Si, Feng Tao, Fei Cai, Zhihong Meng

{"title":"The role of ACSL4 in stroke: mechanisms and potential therapeutic target.","authors":"Bifang Zhuo, Chenyang Qin, Shizhe Deng, Hailun Jiang, Shangkun Si, Feng Tao, Fei Cai, Zhihong Meng","doi":"10.1007/s11010-024-05150-6","DOIUrl":"https://doi.org/10.1007/s11010-024-05150-6","url":null,"abstract":"Stroke, as a neurological disorder with a poor overall prognosis, has long plagued the patients. Current stroke therapy lacks effective treatments. Ferroptosis has emerged as a prominent subject of discourse across various maladies in recent years. As an emerging therapeutic target, notwithstanding its initial identification in tumor cells associated with brain diseases, it has lately been recognized as a pivotal factor in the pathological progression of stroke. Acyl-CoA synthetase long-chain family member 4 (ACSL4) is a potential target and biomarker of catalytic unsaturated fatty acids mediating ferroptosis in stroke. Specifically, the upregulation of ACSL4 leads to heightened accumulation of lipid peroxidation products and reactive oxygen species (ROS), thereby exacerbating the progression of ferroptosis in neuronal cells. ACSL4 is present in various tissues and involved in multiple pathways of ferroptosis. At present, the pharmacological mechanisms of targeting ACSL4 to inhibit ferroptosis have been found in many drugs, but the molecular mechanisms of targeting ACSL4 are still in the exploratory stage. This paper introduces the physiopathological mechanism of ACSL4 and the current status of the research involved in ferroptosis crosstalk and epigenetics, and summarizes the application status of ACSL4 in modern pharmacology research, and discusses the potential application value of ACSL4 in the field of stroke.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142575001","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}

引用次数: 0

O-GlcNAcylation of hexokinase 2 modulates mitochondrial dynamics and enhances the progression of lung cancer. 己糖激酶 2 的 O-GlcNAcylation 可调节线粒体动力学并促进肺癌的进展。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2024-11-04 DOI: 10.1007/s11010-024-05146-2

S I Panpan, G E Wei, W U Kaiming, Renquan Zhang

{"title":"O-GlcNAcylation of hexokinase 2 modulates mitochondrial dynamics and enhances the progression of lung cancer.","authors":"S I Panpan, G E Wei, W U Kaiming, Renquan Zhang","doi":"10.1007/s11010-024-05146-2","DOIUrl":"https://doi.org/10.1007/s11010-024-05146-2","url":null,"abstract":"Non-small cell lung cancer (NSCLC) stands as the prevailing manifestation of lung cancer, with current therapeutic modalities linked to a dismal prognosis, necessitating further advancements. Hexokinase 2 (HK2), a critical enzyme positioned on the mitochondrial membrane, exerts control over diverse biological pathways, thereby regulating cancer. Nevertheless, the precise role and mechanism of HK2 in NSCLC remain inadequately elucidated, warranting comprehensive investigation. HK2 expression in NSCLC tissues and cell lines was detected through immunohistochemistry and western blot analysis. Concurrently, shRNA assays were applied to scrutinize the impact of HK2 on cell proliferation, apoptosis, migration, and invasion processes in NSCLC cell lines, utilizing CCK8, flow cytometry, wound-healing assay, and transwell techniques. The involvement of HK2 in mitochondrial dynamics was probed through western blot analysis, mitochondrial membrane potential assay, and assessment of ROS generation. Next, the functional role of HK2 was assessed by examining its influence on xenograft tumor growth in nude mice in vivo. Further research has demonstrated that HK2 played a role in NSCLC through its O-GlcNAcylation process. The results of the study revealed that HK2 O-GlcNAcylation promoted the proliferation, migration, and invasive characteristics of NSCLC cells, while alleviating mitochondrial damage, whereas O-GlcNAcylation inactivation yielded the opposite effect. Furthermore, in vivo experiments in nude mice illustrated that HK2 O-GlcNAcylation could stimulate tumor growth in NSCLC. These results suggested that HK2 may impact mitochondrial dynamics in NSCLC through its O-GlcNAcylation, thereby contributing to the progression of NSCLC.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142574859","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}

引用次数: 0

Computational insights into NIMA-related kinase 6: unraveling mutational effects on structure and function. 对 NIMA 相关激酶 6 的计算洞察：揭示突变对结构和功能的影响。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2024-11-01 Epub Date: 2023-12-20 DOI: 10.1007/s11010-023-04910-0

Nagesh Kishan Panchal, Shruti Mohanty, Sabina Evan Prince

{"title":"Computational insights into NIMA-related kinase 6: unraveling mutational effects on structure and function.","authors":"Nagesh Kishan Panchal, Shruti Mohanty, Sabina Evan Prince","doi":"10.1007/s11010-023-04910-0","DOIUrl":"10.1007/s11010-023-04910-0","url":null,"abstract":"The NEK6 (NIMA-related kinase 6) serine/threonine kinase is a pivotal player in a multitude of cellular processes, including the regulation of the cell cycle and the response to DNA damage. Its significance extends to disease pathogenesis, as changes in NEK6 activity have been linked to the development of cancer. Non-synonymous single nucleotide polymorphisms (nsSNPs) in NEK6 have been linked to cancer as they alter the protein's native structure and function. The association between NEK6 activity and cancer development has prompted researchers to explore the effects of genetic variations within the NEK6 gene. Therefore, we utilized advanced computational tools to analyze 155 high-confidence nsSNPs in the NEK6 gene. From this analysis, 21 nsSNPs were identified as potentially harmful, raising concerns about their impact on NEK6 activity and cancer risk. These 21 mutations were then examined for structural alterations, and eight of nsSNPs (I51M, V76A, I134N, Y152D, R171Q, V186G, L237R, and C285S) were found to destabilize the protein. Among the destabilizing mutations screened, a specific mutation, R171Q, stood out due to its conserved nature. To understand its impact on the protein and conformation, all-atom molecular dynamics simulations (MDS) for 100 ns were performed for both Wildtype NEK6 (WT-NEK6) and R171Q. The simulations revealed that the R171Q variant was unstable and led to significant conformational changes in NEK6. This study provides valuable insights into NEK6 dysfunction caused by single amino acid alterations, offering a novel understanding of the molecular mechanisms underlying NEK6-related cancer progression.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138807255","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}

引用次数: 0

N6-methyladenosine-induced miR-182-5p promotes multiple myeloma tumorigenesis by regulating CAMK2N1. N6-甲基腺苷诱导的miR-182-5p通过调节CAMK2N1促进多发性骨髓瘤肿瘤发生

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2024-11-01 Epub Date: 2024-01-05 DOI: 10.1007/s11010-023-04906-w

Jing Bao, Tingting Xu, Wanjie Wang, Han Xu, Xiaowen Chen, Ruixiang Xia

{"title":"N6-methyladenosine-induced miR-182-5p promotes multiple myeloma tumorigenesis by regulating CAMK2N1.","authors":"Jing Bao, Tingting Xu, Wanjie Wang, Han Xu, Xiaowen Chen, Ruixiang Xia","doi":"10.1007/s11010-023-04906-w","DOIUrl":"10.1007/s11010-023-04906-w","url":null,"abstract":"Methyltransferase like 3 (METTL3) has been reported to promote tumorigenesis of multiple myeloma (MM), however, the molecular mechanism still needs further research. The N6-methyladenosine (m6A) level in tissues or cells was measured by m6A kit and dot blot assay. The mRNA and protein expression were detected by quantitative real-time PCR (RT-qPCR) and Western blot, respectively. The cell counting kit-8 and colony formation assay were used to detect the cell proliferation. Coimmunoprecipitation (Co-IP) experiment verified the binding of two proteins. The luciferase reporter experiment demonstrated the targeted binding of miR-182-5p and CaMKII inhibitor 1 (CAMK2N1). More importantly, tumor growth was measured in xenograft mice. Our data showed that the expression of METTL3 was significantly increased in MM patients' samples and MM cells. METTL3 overexpression promoted MM cells proliferation, and METTL3 knockdown inhibited MM cells proliferation. Mechanically, METTL3-dependent m6A participated in DiGeorge syndrome critical region 8 (DGCR8)-mediated maturation of pri-miR-182. Upregulation of miR-182-5p further enhanced the promoting proliferation effect of METTL3 overexpression on MM cells. Moreover, the luciferase reporter gene experiment proved that miR-182-5p targetedly regulated CAMK2N1 expression. Xenograft tumor in nude mice further verified that METTL3 promoted MM tumor growth through miR-182/CAMK2N1 signal axis. In summary, the METTL3/miR-182-5p/CAMK2N1 axis plays an important role in MM tumorigenesis, which may provide a new target for MM therapy.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139098233","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}

引用次数: 0

Deciphering the roles of cellular and extracellular non-coding RNAs in chemotherapy-induced cardiotoxicity. 解密细胞和细胞外非编码 RNA 在化疗诱导的心脏毒性中的作用。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2024-11-01 DOI: 10.1007/s11010-024-05143-5

Pan Feng, Fan Yang, Dongmei Zang, Dapeng Bai, Liyan Xu, Yueyun Fu, Ranran You, Tao Liu, Xinyu Yang

{"title":"Deciphering the roles of cellular and extracellular non-coding RNAs in chemotherapy-induced cardiotoxicity.","authors":"Pan Feng, Fan Yang, Dongmei Zang, Dapeng Bai, Liyan Xu, Yueyun Fu, Ranran You, Tao Liu, Xinyu Yang","doi":"10.1007/s11010-024-05143-5","DOIUrl":"https://doi.org/10.1007/s11010-024-05143-5","url":null,"abstract":"Chemotherapy-induced cardiotoxicity is a major adverse effect, driven by multiple factors in its pathogenesis. Notably, RNAs have emerged as significant contributors in both cancer and heart failure (HF). RNAs carry genetic and metabolic information that mirrors the current state of cells, making them valuable as potential biomarkers and therapeutic tools for diagnosing, predicting, and treating a range of diseases, including cardiotoxicity. Over 97% of the genome is transcribed into non-coding RNAs (ncRNAs), including ribosomal RNA (rRNAs), transfer RNAs (tRNAs), and newly identified microRNAs (miRNAs), circular RNAs (circRNAs), and long non-coding RNAs (lncRNAs). NcRNAs function not only within their originating cells but also in recipient cells by being transported through extracellular compartments, referred to as extracellular RNAs (exRNAs). Since ncRNAs were identified as key regulators of gene expression, numerous studies have highlighted their significance in both cancer and cardiovascular diseases. Nevertheless, the role of ncRNAs in cardiotoxicity remains not fully elucidated. The study aims to review the existing knowledge on ncRNAs in Cardio-Oncology and explore the potential of ncRNA-based biomarkers and therapies. These investigations could advance the clinical application of ncRNA research, improving early detection and mitigating of chemotherapy-induced cardiotoxicity.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142562424","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}

引用次数: 0

Triphenyltin isoselenocyanate: a novel nuclear retinoid X receptor ligand with antiproliferative and cytotoxic properties in cell lines derived from human breast cancer. 三苯基锡异硒氰酸酯：一种新型核视黄醇 X 受体配体，在人类乳腺癌细胞系中具有抗增殖和细胞毒性特性。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2024-11-01 Epub Date: 2024-01-16 DOI: 10.1007/s11010-023-04914-w

Dana Macejova, Jakub Kollar, Pavel Bobal, Jan Otevrel, Daniela Schuster, Julius Brtko

{"title":"Triphenyltin isoselenocyanate: a novel nuclear retinoid X receptor ligand with antiproliferative and cytotoxic properties in cell lines derived from human breast cancer.","authors":"Dana Macejova, Jakub Kollar, Pavel Bobal, Jan Otevrel, Daniela Schuster, Julius Brtko","doi":"10.1007/s11010-023-04914-w","DOIUrl":"10.1007/s11010-023-04914-w","url":null,"abstract":"Several commercially available triorganotin compounds were previously found to function as agonist ligands for nuclear retinoid X receptor (RXR) molecules. Triphenyltin isoselenocyanate (TPT-NCSe), a novel selenium atom containing a derivative of triorganotin origin, was found to represent a new cognate bioactive ligand for RXRs. TPT-NCSe displayed a concentration- and time-dependent decrease in the cell viability in both human breast carcinoma MCF-7 (estrogen receptor positive) and MDA‑MB‑231 (triple negative) cell lines. Reactive oxygen species levels generated in response to TPT-NCSe were significantly higher in both carcinoma cell lines treated with TPT-NCSe when compared to mock-treated samples. Treatment with 500 nM TPT-NCSe caused a decrease in SOD1 and increased SOD2 mRNA in MCF-7 cells. The levels of SOD2 mRNA were more increased following the treatment with TPT-NCSe along with 1 μM all-trans retinoic acid (AtRA) in MCF-7 cells. An increased superoxide dismutase SOD1 and SOD2 mRNA levels were also detected in combination treatment of 500 nM TPT-NCSe and 1 μM AtRA in TPT-NCSe-treated MDA-MB-231 cells. The data have also shown that TPT-NCSe induces apoptosis via a caspase cascade triggered by the mitochondrial apoptotic pathway. TPT-NCSe modulates the expression levels of apoptosis‑related proteins, Annexin A5, Bcl‑2 and BAX family proteins, and finally, it enhances the expression levels of its cognate nuclear receptor subtypes RXRalpha and RXRbeta.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11473623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139472759","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}

引用次数: 0

The role of WWP1 and WWP2 in bone/cartilage development and diseases. WWP1 和 WWP2 在骨/软骨发育和疾病中的作用。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2024-11-01 Epub Date: 2024-01-22 DOI: 10.1007/s11010-023-04917-7

Ying Wang, Zuping Wu, Cunyi Wang, Na Wu, Chenyu Wang, Shiyu Hu, Jiejun Shi

引用次数: 0

Relevance and mechanism of STAT3/miR-221-3p/Fascin-1 axis in EGFR TKI resistance of triple-negative breast cancer. STAT3/miR-221-3p/Fascin-1轴在三阴性乳腺癌表皮生长因子受体TKI耐药中的相关性和机制

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2024-11-01 Epub Date: 2023-12-25 DOI: 10.1007/s11010-023-04907-9

Lu-Lu Jin, Hua-Jun Lu, Jun-Kang Shao, Yan Wang, Shi-Ping Lu, Bi-Fei Huang, Gui-Nv Hu, Hong-Chuan Jin, Chao-Qun Wang

{"title":"Relevance and mechanism of STAT3/miR-221-3p/Fascin-1 axis in EGFR TKI resistance of triple-negative breast cancer.","authors":"Lu-Lu Jin, Hua-Jun Lu, Jun-Kang Shao, Yan Wang, Shi-Ping Lu, Bi-Fei Huang, Gui-Nv Hu, Hong-Chuan Jin, Chao-Qun Wang","doi":"10.1007/s11010-023-04907-9","DOIUrl":"10.1007/s11010-023-04907-9","url":null,"abstract":"The epidermal growth factor receptor 1 (EGFR) plays a crucial role in the progression of various malignant tumors and is considered a potential target for treating triple-negative breast cancer (TNBC). However, the effectiveness of representative tyrosine kinase inhibitors (TKIs) used in EGFR-targeted therapy is limited in TNBC patients. In our study, we observed that the TNBC cell lines MDA-MB-231 and MDA-MB-468 exhibited resistance to Gefitinib. Treatment with Gefitinib caused an upregulation of Fascin-1 (FSCN1) protein expression and a downregulation of miR-221-3p in these cell lines. However, sensitivity to Gefitinib was significantly improved in both cell lines with either inhibition of FSCN1 expression or overexpression of miR-221-3p. Our luciferase reporter assay confirmed that FSCN1 is a target of miR-221-3p. Moreover, Gefitinib treatment resulted in an upregulation of phosphorylated signal transducer and activator of transcription 3 (p-STAT3) in MDA-MB-231 cells. Using Stattic, a small-molecule inhibitor of STAT3, we observed a significant enhancement in the inhibitory effect of Gefitinib on the growth, migration, and invasion of MDA-MB-231 cells. Additionally, Stattic treatment upregulated miR-221-3p expression and downregulated FSCN1 mRNA and protein expression. A strong positive correlation was noted between the expression of STAT3 and FSCN1 in breast cancer tissues. Furthermore, patients with high expression levels of both STAT3 and FSCN1 had a worse prognosis. Our findings suggest that elevated FSCN1 expression is linked to primary resistance to EGFR TKIs in TNBC. Moreover, we propose that STAT3 regulates the expression of miR-221-3p/FSCN1 and therefore modulates resistance to EGFR TKI therapy in TNBC. Combining EGFR TKI therapy with inhibition of FSCN1 or STAT3 may offer a promising new therapeutic option for TNBC.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139032449","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}

引用次数: 0

Vitamin D accelerates the subdural hematoma clearance through improving the meningeal lymphatic vessel function. 维生素 D 可通过改善脑膜淋巴管功能加速硬膜下血肿清除。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2024-11-01 Epub Date: 2024-01-31 DOI: 10.1007/s11010-023-04918-6

Yupeng Chen, Xuanhui Liu, Jiangyuan Yuan, Shiying Dong, Meng Nie, Weiwei Jiang, Di Wu, Mingqi Liu, Tao Liu, Chenrui Wu, Chuang Gao, Jianning Zhang, Rongcai Jiang

{"title":"Vitamin D accelerates the subdural hematoma clearance through improving the meningeal lymphatic vessel function.","authors":"Yupeng Chen, Xuanhui Liu, Jiangyuan Yuan, Shiying Dong, Meng Nie, Weiwei Jiang, Di Wu, Mingqi Liu, Tao Liu, Chenrui Wu, Chuang Gao, Jianning Zhang, Rongcai Jiang","doi":"10.1007/s11010-023-04918-6","DOIUrl":"10.1007/s11010-023-04918-6","url":null,"abstract":"Subdural hematoma (SDH) drains into the extracranial lymphatic system through the meningeal lymphatic vessels (mLVs) but the formation of SDH impairs mLVs. Because vitamin D (Vit D) can protect the endothelial cells, we hypothesized that Vit D may enhance the SDH clearance. SDH was induced in Sprague-Dawley rats and treated with Vit D or vehicle. Hematoma volume in each group was measured by H&E staining and hemoglobin quantification. Evans blue (EB) quantification and red blood cells injection were used to evaluated the drainage of mLVs. Western blot analysis and immunofluorescence were conducted to assess the expression of lymphatic protein markers. We also examined the inflammatory factors levels in subdural space by ELISA. Vit D treatment significantly reduced SDH volume and improved the drainage of SDH to cervical lymph nodes. The structure of mLVs in SDH rats were protected by Vit D, and the expressions of LYVE1, PROX1, FOXC2, and VE-cadherin were increased after Vit D treatment. The TNF-α, IL-6, and IL-8 levels were reduced in Vit D group. In vitro, Vit D also increased the VE-cadherin expression levels under inflammation. Vit D protects the structure of mLVs and enhances the absorption of SDH, partly by the anti-inflammatory effect of Vit D.","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":null,"pages":null},"PeriodicalIF":3.5,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139642503","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}

引用次数: 0

PTBP1 as a potential regulator of disease. 作为疾病潜在调节因子的 PTBP1。

IF 3.5 2区生物学

Molecular and Cellular Biochemistry Pub Date : 2024-11-01 Epub Date: 2023-12-22 DOI: 10.1007/s11010-023-04905-x

Qi Yu, Tongtong Wu, Wenhong Xu, Junyuan Wei, Anqi Zhao, Miaomiao Wang, Meiying Li, Guangfan Chi

引用次数: 0