SARS-CoV-2 infection of human iPSC-derived cardiac cells reflects cytopathic features in hearts of patients with COVID-19.
SARS-CoV-2 infection of human iPSC-derived cardiac cells reflects cytopathic features in hearts of patients with COVID-19.
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人IPSC衍生的心脏细胞的SARS-COV-2感染反映了COVID-19患者心脏的细胞病变特征。
DOI：
10.1126/scitranslmed.abf7872
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发表时间：
2021-04-21
影响因子：
17.1
通讯作者：
McDevitt TC
中科院分区：
文献类型：
--
作者：
Perez-Bermejo JA;Kang S;Rockwood SJ;Simoneau CR;Joy DA;Silva AC;Ramadoss GN;Flanigan WR;Fozouni P;Li H;Chen PY;Nakamura K;Whitman JD;Hanson PJ;McManus BM;Ott M;Conklin BR;McDevitt TC
尽管冠状病毒病2019(新冠肺炎)导致高达25%的患者心功能不全，但其发病机制仍不清楚。人诱导多能干细胞(IPSC)来源的心脏细胞暴露于严重急性呼吸综合征冠状病毒2型(SARS-CoV-2)后，显示出生产性感染以及强大的转录和形态损伤特征，尤其是在心肌细胞中。结构基因的转录中断证实了不利的形态特征，包括明显的肌原纤维碎裂和核破坏。来自新冠肺炎患者的人类尸检样本也反映了类似的变化，特别是肌节碎裂。心肌细胞的这些显著的细胞病变特征为深入了解SARS-CoV-2诱导的心脏损伤提供了一个平台，为发现潜在的治疗方法提供了平台，并引发了人们对新冠肺炎在无症状和严重病例中的长期后果的担忧。SARS-CoV-2感染人IPSC来源的心肌细胞导致患者尸检样本中反映出特定的细胞病变特征。
Although coronavirus disease 2019 (COVID-19) causes cardiac dysfunction in up to 25% of patients, its pathogenesis remains unclear. Exposure of human induced pluripotent stem cell (iPSC)-derived heart cells to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) revealed productive infection and robust transcriptomic and morphological signatures of damage, particularly in cardiomyocytes. Transcriptomic disruption of structural genes corroborates adverse morphologic features, which included a distinct pattern of myofibrillar fragmentation and nuclear disruption. Human autopsy specimens from patients with COVID-19 reflected similar alterations, particularly sarcomeric fragmentation. These striking cytopathic features in cardiomyocytes provide insights into SARS-CoV-2-induced cardiac damage, offer a platform for discovery of potential therapeutics, and raise concerns about the long-term consequences of COVID-19 in asymptomatic as well as severe cases. Infection of human iPSC-derived cardiomyocytes by SARS-CoV-2 leads to specific cytopathic features reflected in patient autopsy samples.
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影响因子：
168.9
作者：
Huang, Chaolin;Wang, Yeming;Cao, Bin
通讯作者：
Cao, Bin
β-核心就是使用溶酶体进行出口，而不是生物合成分泌途径。
影响因子：
64.5
作者：
Ghosh S;Dellibovi-Ragheb TA;Kerviel A;Pak E;Qiu Q;Fisher M;Takvorian PM;Bleck C;Hsu VW;Fehr AR;Perlman S;Achar SR;Straus MR;Whittaker GR;de Haan CAM;Kehrl J;Altan-Bonnet G;Altan-Bonnet N
通讯作者：
Altan-Bonnet N
多器官感染和SAR的发病机理。
影响因子：
15.3
作者：
Gu, Jiang;Gong, Encong;Zhang, Bo;Zheng, Jie;Gao, Zifen;Zhong, Yanfeng;Zou, Wanzhong;Zhan, Jun;Wang, Shenglan;Xie, Zhigang;Zhuang, Hui;Wu, Bingquan;Zhong, Haohao;Shao, Hongquan;Fang, Weigang;Gao, Dongshia;Pei, Fei;Li, Xingwang;He, Zhongpin;Xu, Danzhen;Shi, Xeying;Anderson, Virginia M;Leong, Anthony S-Y
通讯作者：
Leong, Anthony S-Y
影响因子：
64.5
作者：
Boersma S;Rabouw HH;Bruurs LJM;Pavlovič T;van Vliet ALW;Beumer J;Clevers H;van Kuppeveld FJM;Tanenbaum ME
通讯作者：
Tanenbaum ME
影响因子：
24
作者：
Giustino G;Croft LB;Stefanini GG;Bragato R;Silbiger JJ;Vicenzi M;Danilov T;Kukar N;Shaban N;Kini A;Camaj A;Bienstock SW;Rashed ER;Rahman K;Oates CP;Buckley S;Elbaum LS;Arkonac D;Fiter R;Singh R;Li E;Razuk V;Robinson SE;Miller M;Bier B;Donghi V;Pisaniello M;Mantovani R;Pinto G;Rota I;Baggio S;Chiarito M;Fazzari F;Cusmano I;Curzi M;Ro R;Malick W;Kamran M;Kohli-Seth R;Bassily-Marcus AM;Neibart E;Serrao G;Perk G;Mancini D;Reddy VY;Pinney SP;Dangas G;Blasi F;Sharma SK;Mehran R;Condorelli G;Stone GW;Fuster V;Lerakis S;Goldman ME
通讯作者：
Goldman ME