JACC: Basic to Translational Science最新文献

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Recognizing Early Career Translational Investigators 表彰早期职业转化研究人员
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2024-10-01 DOI: 10.1016/j.jacbts.2024.09.001
{"title":"Recognizing Early Career Translational Investigators","authors":"","doi":"10.1016/j.jacbts.2024.09.001","DOIUrl":"10.1016/j.jacbts.2024.09.001","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":8.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142530099","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Viewing Pulmonary Arterial Hypertension Pathogenesis and Opportunities for Disease-Modifying Therapy Through the Lens of Biomass 从生物质角度看肺动脉高压发病机制和疾病调节疗法的机遇
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2024-10-01 DOI: 10.1016/j.jacbts.2024.04.009
{"title":"Viewing Pulmonary Arterial Hypertension Pathogenesis and Opportunities for Disease-Modifying Therapy Through the Lens of Biomass","authors":"","doi":"10.1016/j.jacbts.2024.04.009","DOIUrl":"10.1016/j.jacbts.2024.04.009","url":null,"abstract":"<div><div>Fibroproliferative remodeling of distal pulmonary arterioles is a cornerstone characteristic of pulmonary arterial hypertension (PAH). Data from contemporary quantitative imaging suggest that anabolic synthesis of macromolecular substrate, defined here as <em>biomass</em>, is the proximate event that causes vascular remodeling via pathogenic changes to DNA, collagen, cytoskeleton, and lipid membranes. Modifying biomass is achievable but requires tilting the balance in favor of endogenous degradation over synthetic pathways in order to advance the first-ever disease-modifying PAH pharmacotherapy. Viewing PAH pathobiology through the lens of biomass represents an opportunity to decipher novel determinants of disease inception and inform interventions that induce reverse remodeling.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":8.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141709733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
PCSK9 Antibodies Treatment Specifically Enhances the Macrophage-specific Reverse Cholesterol Transport Pathway in Heterozygous Familial Hypercholesterolemia PCSK9 抗体治疗特异性地增强了杂合子家族性高胆固醇血症患者巨噬细胞特异性胆固醇逆向转运途径的功能
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2024-10-01 DOI: 10.1016/j.jacbts.2024.06.008
{"title":"PCSK9 Antibodies Treatment Specifically Enhances the Macrophage-specific Reverse Cholesterol Transport Pathway in Heterozygous Familial Hypercholesterolemia","authors":"","doi":"10.1016/j.jacbts.2024.06.008","DOIUrl":"10.1016/j.jacbts.2024.06.008","url":null,"abstract":"<div><div>We investigated the potential of proprotein convertase subtilisin/kexin type 9 (PCSK9) antibodies to restore macrophage cholesterol efflux in subjects with heterozygous familial hypercholesterolemia (FH) and to enhance the macrophage-specific reverse cholesterol transport pathway in mice. Analyses of macrophage-derived cholesterol distribution of plasma from FH patients revealed that low-density lipoprotein (LDL) particles contained less, and high-density lipoprotein particles contained more radiolabeled cholesterol after treatment with either PCSK9 inhibitor. PCSK9 antibodies facilitated the transfer of macrophage-derived cholesterol and LDL-derived cholesterol to feces exclusively in heterozygous LDL receptor-deficient mice expressing human APOB100. PCSK9 inhibitors act as positive regulators of the macrophage-specific reverse cholesterol transport pathway in individuals with heterozygous FH.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":8.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142530093","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Structure-Based Probe Reveals the Presence of Large Transthyretin Aggregates in Plasma of ATTR Amyloidosis Patients 基于结构的探针揭示了 ATTR 淀粉样变性患者血浆中存在大量的转甲状腺素聚集体
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.05.013
{"title":"Structure-Based Probe Reveals the Presence of Large Transthyretin Aggregates in Plasma of ATTR Amyloidosis Patients","authors":"","doi":"10.1016/j.jacbts.2024.05.013","DOIUrl":"10.1016/j.jacbts.2024.05.013","url":null,"abstract":"<div><div>Amyloidogenic transthyretin (ATTR) amyloidosis is a relentlessly progressive disease caused by the misfolding and systemic accumulation of amyloidogenic transthyretin into amyloid fibrils. These fibrils cause diverse clinical phenotypes, mainly cardiomyopathy and/or polyneuropathy. Little is known about the aggregation of transthyretin during disease development and whether this has implications for diagnosis and treatment. Using the cryogenic electron microscopy structures of mature ATTR fibrils, we developed a peptide probe for fibril detection. With this probe, we have identified previously unknown aggregated transthyretin species in plasma of patients with ATTR amyloidosis. These species are large, non-native, and distinct from monomeric and tetrameric transthyretin. Observations from our study open many questions about the biology of ATTR amyloidosis and reveal a potential diagnostic and therapeutic target.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":8.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24002201/pdfft?md5=5b6a105e3917c13332161203cd4e2112&pid=1-s2.0-S2452302X24002201-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142248574","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Recognizing Early Career Translational Investigators 表彰早期职业转化研究人员
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.07.010
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引用次数: 0
Large Transthyretin Aggregates in Plasma of ATTR Amyloidosis Patients ATTR 淀粉样变性患者血浆中的大颗粒转甲状腺素聚集体
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.07.005
{"title":"Large Transthyretin Aggregates in Plasma of ATTR Amyloidosis Patients","authors":"","doi":"10.1016/j.jacbts.2024.07.005","DOIUrl":"10.1016/j.jacbts.2024.07.005","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":8.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24002626/pdfft?md5=e77b10104ae3c22d7d1194e17b18a735&pid=1-s2.0-S2452302X24002626-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142310564","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway TRIM55 通过调节 Nrf2/HO-1 通路加剧心肌梗死后的心肌细胞凋亡
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.05.006
{"title":"TRIM55 Aggravates Cardiomyocyte Apoptosis After Myocardial Infarction via Modulation of the Nrf2/HO-1 Pathway","authors":"","doi":"10.1016/j.jacbts.2024.05.006","DOIUrl":"10.1016/j.jacbts.2024.05.006","url":null,"abstract":"<div><div>Tripartite motif-containing 55 (Trim55) is mainly expressed in myocardium and skeletal muscle, which plays an important role in promoting the embryonic development of the mouse heart. We investigated the role of Trim55 in myocardial infarction and the associated molecular mechanisms. We studied both gain and loss of function in vivo and in vitro. The results showed that Trim55 knockout improved cardiac function and apoptosis after myocardial infarction, and overexpression aggravated cardiac function damage. The mechanism is that Trim55 interacts with nuclear factor, erythroid derived 2 (Nrf2) to accelerate its degradation and inhibit the expression of heme oxygenase 1, thereby promoting cardiomyocyte apoptosis.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":8.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24002134/pdfft?md5=017379718d1c2bd24f63c67d39e1d9dd&pid=1-s2.0-S2452302X24002134-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142248573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Interferon Interrupted 干扰素中断
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.06.011
{"title":"Interferon Interrupted","authors":"","doi":"10.1016/j.jacbts.2024.06.011","DOIUrl":"10.1016/j.jacbts.2024.06.011","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":8.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24002584/pdfft?md5=86065a350c4da9c923fbf43df31edbe8&pid=1-s2.0-S2452302X24002584-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142310566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Inhibiting the P2Y12 Receptor in Megakaryocytes and Platelets Suppresses Interferon-Associated Responses 抑制巨核细胞和血小板中的 P2Y12 受体可抑制干扰素相关反应
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.05.014
{"title":"Inhibiting the P2Y12 Receptor in Megakaryocytes and Platelets Suppresses Interferon-Associated Responses","authors":"","doi":"10.1016/j.jacbts.2024.05.014","DOIUrl":"10.1016/j.jacbts.2024.05.014","url":null,"abstract":"<div><div>The authors investigated the impact of antiplatelet therapy on the megakaryocyte (MK) and platelet transcriptome. RNA-sequencing was performed on MKs treated with aspirin or P2Y<sub>12</sub> inhibitor, platelets from healthy volunteers receiving aspirin or P2Y<sub>12</sub> inhibition, and platelets from patients with systemic lupus erythematosus (SLE). P2Y<sub>12</sub> inhibition reduced gene expression and inflammatory pathways in MKs and platelets. In SLE, the interferon (IFN) pathway was elevated. In vitro experiments demonstrated the role of P2Y<sub>12</sub> inhibition in reducing IFNα-induced platelet-leukocyte interactions and IFN signaling pathways. These results suggest that P2Y<sub>12</sub> inhibition may have therapeutic potential for proinflammatory and autoimmune conditions like SLE.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":8.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24002213/pdfft?md5=7f2c6a99acc7a7dc4600a00905868755&pid=1-s2.0-S2452302X24002213-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141840267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
Proteomic Profile of the ICAM1 p.K56M HFpEF Risk Variant ICAM1 p.K56M HFpEF 风险变异体的蛋白质组概况
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.05.016
{"title":"Proteomic Profile of the ICAM1 p.K56M HFpEF Risk Variant","authors":"","doi":"10.1016/j.jacbts.2024.05.016","DOIUrl":"10.1016/j.jacbts.2024.05.016","url":null,"abstract":"<div><div>A common missense variant in <em>ICAM1</em> among African American individuals (rs5491; pK56M) has been associated with risk of heart failure with preserved ejection fraction (HFpEF), but the pathways that lead to HFpEF among those with this variant are not clear. In this analysis of 92 circulating proteins and their associated networks, we identified 7 circulating inflammatory proteins associated with rs5491 among &gt;600 African American individuals. Using weighted coexpression network analysis, 3 protein networks were identified, one of which was associated with rs5491. This protein network was most highly represented by members of the tumor necrosis receptor superfamily. The rs5491 variant demonstrated an inflammatory proteomic profile in a separate cohort of African American individuals. This analysis identifies inflammatory pathways that may drive HFpEF among African American individuals with the <em>ICAM1</em> pK56M (rs5491) variant.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":null,"pages":null},"PeriodicalIF":8.4,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2452302X24002262/pdfft?md5=6a8e1da15f7d8bf280efb89154fd82d8&pid=1-s2.0-S2452302X24002262-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142248572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"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
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