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Updated: Oct 1, 2025

Generation of Murine Cardiac Pacemaker Cell Aggregates Based on ES-Cell-Programming in Combination with Myh6-Promoter-Selection
Published on: February 17, 2015
SARS-CoV-2 Infection Induces Ferroptosis of Sinoatrial Node Pacemaker Cells
Yuling Han1, Jiajun Zhu1, Liuliu Yang1
1Department of Surgery (Y.H., J.Z., L.Y., R.H., L.A.L., W.J.S., X.D., T.E., S.C.), Weill Cornell Medicine, New York, NY.
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects heart pacemaker cells, causing dysfunction and ferroptosis. Researchers identified deferoxamine and imatinib as potential drugs to protect sinoatrial node cells from infection.
Area of Science:
- Cardiology
- Virology
- Stem Cell Biology
Background:
- Cardiac arrhythmias are common in COVID-19.
- Human sinoatrial node (SAN) cell research is limited.
- Embryonic stem cells (ESCs) offer a model for SAN cells.
Purpose of the Study:
- Investigate SARS-CoV-2 impact on heart pacemaker cells.
- Model SAN cell infection using human ESCs.
- Identify potential therapeutic interventions.
Main Methods:
- Used a hamster model and human ESC-derived SAN-like cells.
- Confirmed SARS-CoV-2 infection via molecular and imaging techniques.
- Performed drug screening to identify protective agents.
Main Results:
- SARS-CoV-2 RNA and protein found in hamster SAN cells.
- Developed functional human SAN-like cells from hESCs.
- Confirmed SARS-CoV-2 infection induces dysfunction and ferroptosis in SAN cells.
- Identified deferoxamine and imatinib as inhibitors of infection and ferroptosis.
Conclusions:
- SARS-CoV-2 infects cardiac pacemaker cells.
- Ferroptosis is a mechanism for COVID-19-related arrhythmias.
- Identified candidate drugs for protecting SAN cells from SARS-CoV-2.
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