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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 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-10-01 DOI: 10.1016/j.jacbts.2024.09.001
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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 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-10-01 DOI: 10.1016/j.jacbts.2024.04.009
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 biomass, 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.
远端肺动脉的纤维增生性重塑是肺动脉高压（PAH）的基本特征。当代定量成像数据表明，大分子底物（此处定义为生物质）的合成代谢是通过 DNA、胶原蛋白、细胞骨架和脂膜的致病性变化导致血管重塑的近因。改变生物质是可以实现的，但需要将天平倾向于内源性降解，而不是合成途径，这样才能推进首次改变疾病的 PAH 药物疗法。从生物质的角度来看待 PAH 病理生物学，是解读疾病发生的新决定因素并为诱导逆向重塑的干预措施提供信息的一个机会。
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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 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-10-01 DOI: 10.1016/j.jacbts.2024.06.008
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.
我们研究了丙蛋白转化酶亚基酶/kexin 9型（PCSK9）抗体恢复杂合子家族性高胆固醇血症（FH）患者巨噬细胞胆固醇外流以及增强小鼠巨噬细胞特异性胆固醇逆向转运途径的潜力。对 FH 患者血浆中巨噬细胞衍生胆固醇分布的分析表明，使用 PCSK9 抑制剂治疗后，低密度脂蛋白（LDL）颗粒所含放射性标记胆固醇较少，而高密度脂蛋白颗粒所含放射性标记胆固醇较多。在表达人类 APOB100 的杂合子低密度脂蛋白受体缺陷小鼠体内，PCSK9 抗体可促进巨噬细胞衍生胆固醇和低密度脂蛋白衍生胆固醇转移到粪便中。PCSK9抑制剂是杂合子FH患者巨噬细胞特异性胆固醇逆向转运途径的积极调节剂。
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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 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.05.013
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.
淀粉样蛋白转甲状腺素（ATTR）淀粉样变性病是一种无情的渐进性疾病，由淀粉样蛋白转甲状腺素的错误折叠和全身蓄积成淀粉样纤维引起。这些纤维导致多种临床表型，主要是心肌病和/或多发性神经病。人们对转甲状腺素在疾病发展过程中的聚集以及这是否会对诊断和治疗产生影响知之甚少。利用成熟 ATTR 纤维的低温电子显微镜结构，我们开发了一种用于纤维检测的肽探针。利用这种探针，我们在 ATTR 淀粉样变性患者的血浆中鉴定出了以前未知的聚合转甲状腺素。这些物质体积大、非原生、与单体和四聚体转甲状腺素不同。我们的研究结果揭示了有关 ATTR 淀粉样变性生物学的许多问题，并揭示了一个潜在的诊断和治疗靶点。
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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 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
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 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.07.005
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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 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.05.006
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.
含三方基序的 55（Trim55）主要在心肌和骨骼肌中表达，在促进小鼠心脏胚胎发育方面发挥着重要作用。我们研究了 Trim55 在心肌梗死中的作用及其相关分子机制。我们对体内和体外的功能增益和丧失进行了研究。结果表明，Trim55敲除可改善心肌梗死后的心功能和细胞凋亡，而过表达则会加重心功能损伤。其机制是Trim55与核因子红细胞衍生2（Nrf2）相互作用，加速其降解并抑制血红素加氧酶1的表达，从而促进心肌细胞凋亡。
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引用次数: 0
Interferon Interrupted 干扰素中断
IF 8.4 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.06.011
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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 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.05.014
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 P2Y12 inhibitor, platelets from healthy volunteers receiving aspirin or P2Y12 inhibition, and platelets from patients with systemic lupus erythematosus (SLE). P2Y12 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 P2Y12 inhibition in reducing IFNα-induced platelet-leukocyte interactions and IFN signaling pathways. These results suggest that P2Y12 inhibition may have therapeutic potential for proinflammatory and autoimmune conditions like SLE.
作者研究了抗血小板疗法对巨核细胞（MK）和血小板转录组的影响。研究人员对接受阿司匹林或P2Y12抑制剂治疗的巨核细胞、接受阿司匹林或P2Y12抑制剂治疗的健康志愿者的血小板以及系统性红斑狼疮（SLE）患者的血小板进行了RNA测序。P2Y12 抑制剂减少了 MKs 和血小板中的基因表达和炎症通路。在系统性红斑狼疮中，干扰素（IFN）通路升高。体外实验证明了 P2Y12 抑制剂在减少 IFNα 诱导的血小板-白细胞相互作用和 IFN 信号通路中的作用。这些结果表明，P2Y12 抑制剂可能对系统性红斑狼疮等促炎性和自身免疫性疾病具有治疗潜力。
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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 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-09-01 DOI: 10.1016/j.jacbts.2024.05.016
A common missense variant in ICAM1 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 >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 ICAM1 pK56M (rs5491) variant.
非裔美国人中一种常见的错义变异（rs5491; pK56M）与射血分数保留型心力衰竭（HFpEF）的风险有关，但导致该变异者发生 HFpEF 的途径尚不清楚。在对 92 种循环蛋白及其相关网络的分析中，我们在超过 600 名非洲裔美国人中发现了 7 种与 rs5491 相关的循环炎症蛋白。通过加权共表达网络分析，我们发现了 3 个蛋白质网络，其中一个与 rs5491 相关。该蛋白质网络中肿瘤坏死受体超家族成员的代表性最高。在一个单独的非裔美国人队列中，rs5491 变体显示出炎症蛋白组特征。这项分析确定了可能驱动具有 pK56M (rs5491) 变体的非裔美国人发生高房血症的炎症途径。
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