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Xie X, Tie YF, Lai S, et al. Cardiac-specific CGI-58 deficiency activates the ER stress pathway to promote heart failure in mice. Cell Death Dis. 2021;12(11):1003doi: 10.1038/s41419-021-04282-7.
Xie, X., Tie, Y. F., Lai, S., Zhang, Y. L., Li, H. H., & Liu, Y. (2021). Cardiac-specific CGI-58 deficiency activates the ER stress pathway to promote heart failure in mice. Cell death & disease, 12(11), 1003. https://doi.org/10.1038/s41419-021-04282-7
Xie, Xin, et al. "Cardiac-specific CGI-58 deficiency activates the ER stress pathway to promote heart failure in mice." Cell death & disease vol. 12,11 (2021): 1003. doi: https://doi.org/10.1038/s41419-021-04282-7
Xie X, Tie YF, Lai S, Zhang YL, Li HH, Liu Y. Cardiac-specific CGI-58 deficiency activates the ER stress pathway to promote heart failure in mice. Cell Death Dis. 2021 Oct 26;12(11):1003. doi: 10.1038/s41419-021-04282-7. PMID: 34702801; PMCID: PMC8548506.
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Cell Death Dis. 2021 Oct 26;12(11):1003. doi: 10.1038/s41419-021-04282-7.

Cardiac-specific CGI-58 deficiency activates the ER stress pathway to promote heart failure in mice.

Cell death & disease

Xin Xie, Yi-Fan Tie, Song Lai, Yun-Long Zhang, Hui-Hua Li, Ying Liu

Affiliations

  1. Department of Cardiology, Institute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, 116011, Dalian, China.
  2. Department of Emergency Medicine, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing Chaoyang Hospital, Capital Medical University, 100020, Beijing, China.
  3. Department of Cardiology, Institute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, 116011, Dalian, China. [email protected].
  4. Department of Emergency Medicine, Beijing Key Laboratory of Cardiopulmonary Cerebral Resuscitation, Beijing Chaoyang Hospital, Capital Medical University, 100020, Beijing, China. [email protected].
  5. Department of Cardiology, Institute of Cardiovascular Diseases, First Affiliated Hospital of Dalian Medical University, 116011, Dalian, China. [email protected].

PMID: 34702801 PMCID: PMC8548506 DOI: 10.1038/s41419-021-04282-7

Abstract

Excess myocardial triacylglycerol accumulation (i.e., cardiac steatosis) impairs heart function, suggesting that enzymes promoting triacylglycerol metabolism exert essential regulatory effects on heart function. Comparative gene identification 58 (CGI-58) is a key enzyme that promotes the hydrolysis of triglycerides by activating adipose triglyceride lipase and plays a protective role in maintaining heart function. In this study, the effects of CGI-58 on heart function and the underlying mechanism were investigated using cardiac-specific CGI58-knockout mice (CGI-58

© 2021. The Author(s).

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