JCI: 肺动脉高压与内皮细胞衰老，Frataxin新发现

2021-09-29 刘少飞 MedSci原创

SophylioJerry

学生/

Frataxin deficiency promotes endothelial senescence in pulmonary hypertension.

Frataxin deficiency promotes endothelial senescence in pulmonary hypertension.

期刊年卷：J Clin Invest 2021 Apr 27;

通讯作者：Stephen Y. Chan, MD, PhD

Director, Center for Pulmonary Vascular Biology and Medicine

Associate Program Director, Cardiology Fellowship Research Program

Professor of Medicine, Division of Cardiology, Department of Medicine，University of Pittsburgh

众所周知，肺动脉高压（PH）中内皮病理表型的动态调节仍未确定。细胞衰老与心内分流引起的PH有关。但是，其对PH亚型的调节尚不清楚。由于内皮细胞缺乏铁硫（Fe-S）簇在PH中是致病的，因此研究假设Fe-S生物发生蛋白frataxin（FXN）控制着内皮的衰老。啮齿动物和患者肺部不同PH类型的内皮细胞亚群表现出FXN减少和衰老增加。在体外，缺氧和炎症性FXN缺乏消除了含内皮Fe-S的聚合酶的活性，从而促进了复制压力，DNA损伤反应和衰老。在来自Friedreich共济失调（FRDA）的干细胞来源的内皮细胞中也观察到这种情况，这是一种FXN缺乏，共济失调和心肌病的遗传疾病，通常伴有PH。在体内，FXN缺乏依赖性衰老驱动血管炎症，重塑和PH，而在缺乏Fxn的啮齿类动物中药理去除衰老细胞可改善PH。这些数据提供了PH中的内皮生物学模型，其中FXN缺乏会产生衰老的内皮亚群，从而促进其他细胞中的血管炎性和增生性信号来驱动疾病。这些发现还建立了FRDA和左心病中PH的内皮病因，并支持麻醉药的治疗发展，逆转了跨PH亚型的Fe-S缺乏症的影响。

总的来说，这项工作提供了一个统一的 Fe-S 依赖性机制，解释了多种 PH 病因中内皮表型的动态进展。该研究描绘了 FRDA 和潜在的其他形式的第二类型的 PH （PHLHD）的内皮特异性 PH 倾向。更广泛地说，该研究研究结果将 FXN 对 Fe-S 生物学、基因组完整性和衰老的调节作用联系起来，并提出了对这种致命疾病进行更有效诊断和治疗的目标。

文章出处：Culley MK. Frataxin deficiency promotes endothelial senescence in pulmonary hypertension. J Clin Invest. 2021 Jun 1;131(11):e136459. doi: 10.1172/JCI136459. PMID: 33905372; PMCID: PMC8159699.

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2022-04-05 jklm09

#动脉高压#

106 0 举报
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2021-10-14 caobinglei8079

#JCI#

96 0 举报
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2022-06-25 vera_1203

#新发现#

97 0 举报
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2021-09-30 ms8543593053280928

#细胞衰老#

155 0 举报
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2021-09-30 bbjsj_1981

#ATA#

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