Translational Research最新文献

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Siglec-5 as a novel receptor mediates endothelial cells oxLDL transcytosis to promote atherosclerosis Siglec-5 作为一种新型受体介导内皮细胞 oxLDL 转运,促进动脉粥样硬化。
IF 6.4 2区 医学
Translational Research Pub Date : 2024-09-26 DOI: 10.1016/j.trsl.2024.09.003
Xiong Jia , Xiangli Bai , Zhiqiang Yin , Qijun Zheng , Yin Zhao , Yajing Lu , Yan Shu , Yayu Wang , Yifei Zhang , Si Jin
{"title":"Siglec-5 as a novel receptor mediates endothelial cells oxLDL transcytosis to promote atherosclerosis","authors":"Xiong Jia ,&nbsp;Xiangli Bai ,&nbsp;Zhiqiang Yin ,&nbsp;Qijun Zheng ,&nbsp;Yin Zhao ,&nbsp;Yajing Lu ,&nbsp;Yan Shu ,&nbsp;Yayu Wang ,&nbsp;Yifei Zhang ,&nbsp;Si Jin","doi":"10.1016/j.trsl.2024.09.003","DOIUrl":"10.1016/j.trsl.2024.09.003","url":null,"abstract":"<div><h3>Background</h3><div>Excessive subendothelial retention of oxidized low-density lipoprotein (oxLDL) and subsequent oxLDL engulfment by macrophages leads to the formation of foam cells and the development of atherosclerosis. Our previous study showed that the plasma level of sialic acid-binding immunoglobulin-like lectin 5 (Siglec-5) was a novel biomarker for the prognosis of atherosclerosis in diabetic patients. However, the role and underlying mechanisms of Siglec-5 in atherosclerosis have not been elucidated.</div></div><div><h3>Methods</h3><div>The interaction between oxLDL and Siglec-5 was detected by fluorescence colocalization and coimmunoprecipitation. The effect of oxLDL on Siglec-5 expression was detected in endothelial cells and macrophages, and the effect of Siglec-5 on oxLDL transcytosis and uptake was investigated. Siglec-5 was overexpressed in mice using recombinant adeno-associated virus vector serotype 9 (rAAV9-Siglec-5) to evaluate the effect of Siglec-5 on oxLDL uptake and atherogenesis <em>in vivo</em>. In addition, the effects of Siglec-5 antibodies and soluble Siglec-5 proteins on oxLDL transcytosis and uptake and their role in atherogenesis were investigated <em>in vivo</em> and <em>in vitro</em>.</div></div><div><h3>Results</h3><div>We found that oxLDL interacted with Siglec-5 and that oxLDL stimulated the expression of Siglec-5. Siglec-5 promotes the transcytosis and uptake of oxLDL, while both anti-Siglec-5 antibodies and soluble Siglec-5 protein attenuated oxLDL transcytosis and uptake. Interestingly, overexpression of Siglec-5 by recombinant adeno-associated viral vector serotype 9 (rAAV9-Siglec-5) promoted the retention of oxLDL in the aorta of C57BL/6 mice. Moreover, overexpression of Siglec-5 significantly accelerated the formation of atherosclerotic lesions in Apoe<sup>−/−</sup> mice. Moreover, both anti-Siglec-5 antibodies and soluble Siglec-5 protein significantly alleviated the retention of oxLDL in the aorta of rAAV9-Siglec-5-transfected C57BL/6 mice and the formation of atherosclerotic plaques in rAAV9-Siglec-5-transfected Apoe<sup>−/−</sup> mice.</div></div><div><h3>Conclusion</h3><div>Our results suggested that Siglec-5 was a novel receptor that mediated oxLDL transcytosis and promoted the formation of foam cells. Interventions that inhibit the interaction between oxLDL and Siglec-5, including anti-Siglec-5 antibody or soluble Siglec-5 protein treatment, may provide novel therapeutic strategies in treating atherosclerosis.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"274 ","pages":"Pages 49-66"},"PeriodicalIF":6.4,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142335634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Diagnostic, prognostic, and predictive biomarkers in gastric cancer: from conventional to novel biomarkers 胃癌的诊断、预后和预测生物标志物:从传统生物标志物到新型生物标志物。
IF 6.4 2区 医学
Translational Research Pub Date : 2024-09-10 DOI: 10.1016/j.trsl.2024.09.001
Ghazaleh Khalili-Tanha , Nima Khalili-Tanha , Arian Karimi Rouzbahani , Ramisa Mahdieh , Kimia Jasemi , Rosa Ghaderi , Fatemeh Khojasteh Leylakoohi , Elnaz Ghorbani , Majid Khazaei , Seyed Mahdi Hassanian , Ibrahim Saeed Gataa , Gordon A Ferns , Elham Nazari , Amir Avan
{"title":"Diagnostic, prognostic, and predictive biomarkers in gastric cancer: from conventional to novel biomarkers","authors":"Ghazaleh Khalili-Tanha ,&nbsp;Nima Khalili-Tanha ,&nbsp;Arian Karimi Rouzbahani ,&nbsp;Ramisa Mahdieh ,&nbsp;Kimia Jasemi ,&nbsp;Rosa Ghaderi ,&nbsp;Fatemeh Khojasteh Leylakoohi ,&nbsp;Elnaz Ghorbani ,&nbsp;Majid Khazaei ,&nbsp;Seyed Mahdi Hassanian ,&nbsp;Ibrahim Saeed Gataa ,&nbsp;Gordon A Ferns ,&nbsp;Elham Nazari ,&nbsp;Amir Avan","doi":"10.1016/j.trsl.2024.09.001","DOIUrl":"10.1016/j.trsl.2024.09.001","url":null,"abstract":"<div><div>Gastric cancer is a major health concern worldwide. The survival rate of Gastric cancer greatly depends on the stage at which it is diagnosed. Early diagnosis is critical for improving survival outcomes. To improve the chances of early diagnosis, regular screening tests, such as an upper endoscopy or barium swallow, are recommended for individuals at a higher risk due to factors like family history or a previous diagnosis of gastric conditions. Biomarkers can be detected and measured using non-invasive methods such as blood tests, urine tests, breath analysis, or imaging techniques. These non-invasive approaches offer many advantages, including convenience, safety, and cost-effectiveness, making them valuable tools for disease diagnosis, monitoring, and research. Biomarker-based tests have emerged as a useful tool for identifying gastric cancer early, monitoring treatment response, assessing the recurrence risk, and personalizing treatment plans. In this current review, we have explored both classical and novel biomarkers for gastric cancer. We have centralized their potential clinical application and discussed the challenges in Gastric cancer research.</div></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"274 ","pages":"Pages 35-48"},"PeriodicalIF":6.4,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142305344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Information for Readers 读者信息
IF 6.4 2区 医学
Translational Research Pub Date : 2024-09-09 DOI: 10.1016/S1931-5244(24)00165-8
{"title":"Information for Readers","authors":"","doi":"10.1016/S1931-5244(24)00165-8","DOIUrl":"10.1016/S1931-5244(24)00165-8","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"273 ","pages":"Page IBC"},"PeriodicalIF":6.4,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142157823","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Author Guidelines 作者指南
IF 6.4 2区 医学
Translational Research Pub Date : 2024-09-09 DOI: 10.1016/S1931-5244(24)00164-6
{"title":"Author Guidelines","authors":"","doi":"10.1016/S1931-5244(24)00164-6","DOIUrl":"10.1016/S1931-5244(24)00164-6","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"273 ","pages":"Pages iii-iv"},"PeriodicalIF":6.4,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142157822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Editorial Advisory Board 编辑顾问委员会
IF 6.4 2区 医学
Translational Research Pub Date : 2024-09-09 DOI: 10.1016/S1931-5244(24)00163-4
{"title":"Editorial Advisory Board","authors":"","doi":"10.1016/S1931-5244(24)00163-4","DOIUrl":"10.1016/S1931-5244(24)00163-4","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"273 ","pages":"Page ii"},"PeriodicalIF":6.4,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1931524424001634/pdfft?md5=a76ad259a7dd427d26d8447389f22bc1&pid=1-s2.0-S1931524424001634-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142157821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
J147 treatment protects against traumatic brain injury by inhibiting neuronal endoplasmic reticulum stress potentially via the AMPK/SREBP-1 pathway J147 可通过 AMPK/SREBP-1 途径抑制神经元内质网应激,从而保护大脑免受创伤性脑损伤。
IF 6.4 2区 医学
Translational Research Pub Date : 2024-09-07 DOI: 10.1016/j.trsl.2024.08.007
Rong Jin , Min Wang , Manish Shukla , Yuguo Lei , Dong An , Jiwen Du , Guohong Li
{"title":"J147 treatment protects against traumatic brain injury by inhibiting neuronal endoplasmic reticulum stress potentially via the AMPK/SREBP-1 pathway","authors":"Rong Jin ,&nbsp;Min Wang ,&nbsp;Manish Shukla ,&nbsp;Yuguo Lei ,&nbsp;Dong An ,&nbsp;Jiwen Du ,&nbsp;Guohong Li","doi":"10.1016/j.trsl.2024.08.007","DOIUrl":"10.1016/j.trsl.2024.08.007","url":null,"abstract":"<div><p>Endoplasmic reticulum (ER) stress is recognized as a crucial contributor to the progression of traumatic brain injury (TBI) and represents a potential target for therapeutic intervention. This study aimed to assess the potential of J147, a novel neurotrophic compound, in alleviating ER stress by modulating related signaling pathways, thereby promoting functional recovery in TBI. To this end, adult mice underwent controlled cortical impact (CCI) injury to induce TBI, followed by oral administration of J147 one-hour post-injury, with daily dosing for 3 to 7 days. Multiple behavioral assessments were conducted over 35 days, revealing a significant, dose-dependent improvement in neurofunctional recovery with J147 treatment. The neuropathological analysis demonstrated reduced acute neurodegeneration (observed at three days through FJC staining), enhanced long-term neuron survival (H&amp;E and Nissl staining), and improved neuroplasticity (Golgi staining) at 35 days post-TBI. At the molecular level, TBIinduced AMP-activated protein kinase (AMPK) dephosphorylation, sterol regulatory element binding protein-1 (SREBP-1) activation, and upregulation of ER stress marker proteins, including phosphorylated eukaryotic initiation factor-2α (p-eIF2a), activating transcription factor 4 (ATF4), and C/EBP homologous protein (CHOP) in perilesional cortex neurons at three days post-injury. Notably, the J147 treatment significantly attenuated AMPK dephosphorylation, SERBP-1 activation, and expression of the ER stress markers. In summary, this study reveals the therapeutic promise of J147 in mitigating secondary brain damage associated with TBI and improving long-term functional recovery by modulating ER stress pathways.</p></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"274 ","pages":"Pages 21-34"},"PeriodicalIF":6.4,"publicationDate":"2024-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142157085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Author Guidelines 作者指南
IF 6.4 2区 医学
Translational Research Pub Date : 2024-09-05 DOI: 10.1016/S1931-5244(24)00157-9
{"title":"Author Guidelines","authors":"","doi":"10.1016/S1931-5244(24)00157-9","DOIUrl":"10.1016/S1931-5244(24)00157-9","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"272 ","pages":"Pages iii-iv"},"PeriodicalIF":6.4,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142148502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Information for Readers 读者信息
IF 6.4 2区 医学
Translational Research Pub Date : 2024-09-05 DOI: 10.1016/S1931-5244(24)00158-0
{"title":"Information for Readers","authors":"","doi":"10.1016/S1931-5244(24)00158-0","DOIUrl":"10.1016/S1931-5244(24)00158-0","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"272 ","pages":"Page IBC"},"PeriodicalIF":6.4,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142148503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Editorial Advisory Board 编辑顾问委员会
IF 6.4 2区 医学
Translational Research Pub Date : 2024-09-05 DOI: 10.1016/S1931-5244(24)00156-7
{"title":"Editorial Advisory Board","authors":"","doi":"10.1016/S1931-5244(24)00156-7","DOIUrl":"10.1016/S1931-5244(24)00156-7","url":null,"abstract":"","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"272 ","pages":"Page ii"},"PeriodicalIF":6.4,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1931524424001567/pdfft?md5=beeb9ea39e3d49bea4bd33c3ae10d3a5&pid=1-s2.0-S1931524424001567-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142148501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
DUSP5 deficiency suppresses the progression of acute kidney injury by enhancing autophagy through AMPK/ULK1 pathway 缺乏 DUSP5 可通过 AMPK/ULK1 途径增强自噬作用,从而抑制急性肾损伤的进展。
IF 6.4 2区 医学
Translational Research Pub Date : 2024-08-30 DOI: 10.1016/j.trsl.2024.08.006
Fang Bai , Chunjie Wang , Sha Wang , Yuxuan Zhao , Feng Feng , Kuipeng Yu , Lei Liu , Xiangdong Yang
{"title":"DUSP5 deficiency suppresses the progression of acute kidney injury by enhancing autophagy through AMPK/ULK1 pathway","authors":"Fang Bai ,&nbsp;Chunjie Wang ,&nbsp;Sha Wang ,&nbsp;Yuxuan Zhao ,&nbsp;Feng Feng ,&nbsp;Kuipeng Yu ,&nbsp;Lei Liu ,&nbsp;Xiangdong Yang","doi":"10.1016/j.trsl.2024.08.006","DOIUrl":"10.1016/j.trsl.2024.08.006","url":null,"abstract":"<div><p>Acute kidney injury (AKI) represents a critical clinical disease characterized by the rapid decline in renal function, carrying a substantial burden of morbidity and mortality. The treatment of AKI is frequently limited by its variable clinical presentations and intricate pathophysiology, highlighting the urgent need for a deeper understanding of its pathogenesis and potential therapeutic targets. Dual-specific protein phosphatase 5 (DUSP5), a member of the serine-threonine phosphatase family, possesses the capability to dephosphorylate extracellular regulated protein kinases (ERK). DUSP5 has emerged as a pivotal player in modulating metabolic signals, inflammatory responses, and cancer progression, while also being closely associated with various kidney diseases. This study systematically scrutinized the function and mechanism of DUSP5 in AKI for the first time, unveiling a substantial increase in DUSP5 expression during AKI. Moreover, DUSP5 knockdown was observed to attenuate the production of inflammatory factors and apoptotic cells in renal tubular epithelial cells by enhancing AMPK/ULK1-mediated autophagy, thus improving renal function. In a word, DUSP5 knockdown in AKI effectively impede disease progression by activating autophagy. This finding holds promise for introducing fresh perspectives and targets for AKI treatment.</p></div>","PeriodicalId":23226,"journal":{"name":"Translational Research","volume":"274 ","pages":"Pages 1-9"},"PeriodicalIF":6.4,"publicationDate":"2024-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142116718","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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