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When Off-Target Is the Target 当脱靶就是目标时
IF 8.4 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-11-01 DOI: 10.1016/j.jacbts.2024.09.012
Jonathan A. Kirk PhD
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引用次数: 0
Targeting Soluble TGF-β Factors 靶向可溶性 TGF-β 因子
IF 8.4 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-11-01 DOI: 10.1016/j.jacbts.2024.04.005
Clarissa Becher MSc , Marius Wits MSc , Frances S. de Man Prof , Gonzalo Sanchez-Duffhues PhD , Marie-Jose Goumans Prof
Pulmonary arterial hypertension (PAH) is a rare progressive disease characterized by pulmonary artery vascular remodeling, increased vascular resistance, and subsequent right ventricular hypertrophy and right heart failure. It is triggered by disrupted transforming growth factor (TGF)-β signaling, including loss-of-function mutations in the bone morphogenetic protein (BMP) receptor 2. Emerging treatments aim to inhibit elevated TGF-β levels or enhance diminished endothelial BMP signaling. This review aims to summarize the role of the TGF-β superfamily in the pathobiology of PAH and recent discoveries highlighting altered expression of TGF-β–related soluble factors in PAH patients that can serve as potential biomarkers and drug targets. The discussion focuses on how these altered factors can guide treatment decisions and monitor therapeutic responses, facilitating personalized patient care through the integration of diagnostics and therapy, that is, precision medicine. This approach tailors treatment strategies to individual patients based on their unique disease characteristics.
肺动脉高压（PAH）是一种罕见的进行性疾病，其特征是肺动脉血管重塑、血管阻力增加以及随后的右心室肥大和右心衰竭。其诱因是转化生长因子（TGF）-β 信号转导紊乱，包括骨形态发生蛋白（BMP）受体 2 的功能缺失突变。新出现的治疗方法旨在抑制升高的 TGF-β 水平或增强减弱的内皮 BMP 信号传导。本综述旨在总结 TGF-β 超家族在 PAH 病理生物学中的作用，以及近期发现的 PAH 患者中与 TGF-β 相关的可溶性因子表达的改变，这些因子可作为潜在的生物标记物和药物靶点。讨论的重点是这些改变的因子如何指导治疗决策和监测治疗反应，通过整合诊断和治疗（即精准医疗）促进个性化患者护理。这种方法可根据患者独特的疾病特征为其量身定制治疗策略。
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引用次数: 0
Non-Cell-Autonomous Cardiomyocyte Regulation Complicates Gene Supplementation Therapy for Lmna-Associated Cardiac Defects in Mice 非细胞自主性心肌细胞调控使小鼠 Lmna 相关心脏缺陷的基因补充疗法变得复杂
IF 8.4 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-11-01 DOI: 10.1016/j.jacbts.2024.06.004
Yueshen Sun MB , Congting Guo BS , Zhan Chen BS , Junsen Lin BS , Luzi Yang MM , Yueyang Zhang BS , Chenyang Wu BS , Dongyu Zhao PhD , Blake Jardin MS , William T. Pu MD , Mingming Zhao PhD , Erdan Dong MD , Xiaomin Hu PhD , Shuyang Zhang MD , Yuxuan Guo PhD
The truncating mutations of LMNA are the major causes of cardiomyopathy. Here we studied 3 mouse models that carry germline, cardiomyocyte-specific, or genetic mosaic Lmna truncating mutations. Whereas the germline mutant manifested cardiac maturation defects, cardiomyocyte-specific mutation triggered pathological hypertrophy. In genetic mosaic analysis, no morphological defects were observed. Three adeno-associated virus (AAV) vectors were applied to addback lamin-A in a ubiquitous, cardiomyocyte-specific, or cardiomyocyte-excluded manner. Strikingly, only ubiquitous and cardiomyocyte-excluded AAV vectors mitigated the cardiac defects. Therefore, Lmna regulates cardiac morphology and function via a non-cell-autonomous mechanism. Noncardiomyocytes are key targets in AAV lamin-A therapy for Lmna-associated cardiac defects.
LMNA 截断突变是心肌病的主要病因。在这里，我们研究了携带种系、心肌细胞特异性或遗传镶嵌Lmna截短突变的3种小鼠模型。种系突变体表现出心脏成熟缺陷，而心肌细胞特异性突变则引发病理性肥大。在基因镶嵌分析中，没有观察到形态学缺陷。应用三种腺相关病毒（AAV）载体，以普遍存在、心肌细胞特异性或心肌细胞排除的方式加回了lamin-A。令人震惊的是，只有无处不在和排除心肌细胞的 AAV 载体能缓解心脏缺陷。因此，Lmna 通过非细胞自主机制调节心脏形态和功能。非心肌细胞是 AAV lamin-A 治疗 Lmna 相关心脏缺陷的关键靶点。
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引用次数: 0
Targeting USP25 in the Heart 瞄准心脏中的 USP25
IF 8.4 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-11-01 DOI: 10.1016/j.jacbts.2024.08.001
Hanming Zhang PhD
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引用次数: 0
Endothelial Shear Stress Metrics Associate With Proinflammatory Pathways at the Culprit Site of Coronary Erosion 内皮剪切应力指标与冠状动脉侵蚀罪魁祸首的促炎途径有关
IF 8.4 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-11-01 DOI: 10.1016/j.jacbts.2024.07.008
Mona E. Ahmed MD, PhD , David M. Leistner MD , Diaa Hakim MD, PhD , Youssef Abdelwahed MD , Ahmet U. Coskun PhD , Charles Maynard PhD , Claudio Seppelt MD , Gregor Nelles MD , Denitsa Meteva MD , Nicholas V. Cefalo BS , Peter Libby MD , Ulf Landmesser MD , Peter H. Stone MD
Low endothelial shear stress (ESS) and associated adverse biomechanical features stimulate inflammation, contribute to atherogenesis, and predispose to coronary plaque disruption. The mechanistic links between adverse flow-related hemodynamics and inflammatory mediators implicated in plaque erosion, however, remain little explored. We investigated the relationship of high-risk ESS metrics to culprit lesion proinflammatory/proatherogenic cells and cytokines/chemokines implicated in coronary plaque erosion in patients with acute coronary syndromes. In eroded plaques, low ESS, high ESS gradient, and steepness of plaque topographical slope associated with increased numbers of local T cells and subsets (CD4+, CD8+, natural killer T cells) as well as inflammatory mediators (interleukin [IL]-6, macrophage inflammatory protein-1β, IL-1β, IL-2).
低内皮剪切应力（ESS）和相关的不良生物力学特征会刺激炎症，导致动脉粥样硬化，并容易造成冠状动脉斑块破坏。然而，与血流相关的不良血流动力学与斑块侵蚀所涉及的炎症介质之间的机理联系仍然鲜有探索。我们研究了急性冠状动脉综合征患者的高风险ESS指标与冠状动脉斑块侵蚀的罪魁祸首病变原炎/致动脉粥样硬化细胞和细胞因子/凝血因子之间的关系。在侵蚀斑块中，低ESS、高ESS梯度和斑块地形坡度的陡度与局部T细胞和亚群（CD4+、CD8+、自然杀伤T细胞）以及炎症介质（白细胞介素[IL]-6、巨噬细胞炎症蛋白-1β、IL-1β、IL-2）数量的增加有关。
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引用次数: 0
Immune Shielding of Human Heart Valves 人体心脏瓣膜的免疫屏蔽
IF 8.4 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
JACC: Basic to Translational Science
Pub Date : 2024-11-01 DOI: 10.1016/j.jacbts.2024.07.003
Marijn C. Peters PhD , Arnaud Zaldumbide PhD , Esmee J. Groeneveld BSc , Martijn J.W.E. Rabelink BSc , Janneke H. Peerlings MSc , Antoon van den Bogaerdt MSc , Carlijn V.C. Bouten PhD , Rob C. Hoeben PhD , Marie-Jose Goumans PhD , Abraham van Wijk MD, PhD
Children born with defective heart valves require multiple donor valve replacements throughout life, because these cannot grow and can cause early failure through immune degeneration. This study tests the lentiviral delivery of viral immune evasion genes US2 and human serpin 9 to shield human heart valves from immune rejection. The results show we can efficiently down-regulate human leukocyte antigen expression in heart valve cells and in intact heart valve tissue resulting in decreased activity of a human leukocyte antigen–reactive CD8+ T-cell clone without inducing cytotoxicity. This study demonstrates immune shielding of human heart valves and brings us closer to a durable valve graft in pediatric patients.
先天性心脏瓣膜有缺陷的儿童一生中需要多次供体瓣膜置换，因为这些瓣膜无法生长，并可能因免疫变性而导致早期衰竭。这项研究测试了慢病毒递送病毒免疫逃避基因 US2 和人类血清素 9 以保护人类心脏瓣膜免受免疫排斥。结果表明，我们可以有效下调心脏瓣膜细胞和完整心脏瓣膜组织中人类白细胞抗原的表达，从而降低人类白细胞抗原反应性 CD8+ T 细胞克隆的活性，而不会诱导细胞毒性。这项研究证明了人类心脏瓣膜的免疫屏蔽作用，使我们更接近于为儿科患者提供持久的瓣膜移植。
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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 : 2024-11-01 DOI: 10.1016/j.jacbts.2024.10.001
Douglas L. Mann MD (Editor-in-Chief: JACC: Basic to Translational Science)
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引用次数: 0
Reverse Translation of Pericardial Access 反向翻译心包通路
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.2024.08.007
Pedro Mendes-Ferreira PhD , André M. Leite-Moreira MD, MS , Adelino F. Leite-Moreira MD, PhD
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引用次数: 0
Charting New Real Estate 绘制新房地产图
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.2024.08.004
Ali Fatehi Hassanabad MD, MSc , Justin F. Deniset PhD , Paul W.M. Fedak MD, PhD
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引用次数: 0
Proteomics of Large Artery Stiffness 大动脉僵化的蛋白质组学研究
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.2024.07.011
Gary F. Mitchell MD
{"title":"Proteomics of Large Artery Stiffness","authors":"Gary F. Mitchell MD","doi":"10.1016/j.jacbts.2024.07.011","DOIUrl":"10.1016/j.jacbts.2024.07.011","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"9 10","pages":"Pages 1192-1194"},"PeriodicalIF":8.4,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142530877","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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