HOTAIR regulates SIRT3-mediated cardiomyocyte survival after myocardial ischemia/reperfusion by interacting with FUS

Jixuan Liu; Mingzhuang Sun; Jinda Wang; Zhijun Sun; Gang Wang

doi:10.1186/s12872-023-03203-0

BMC Cardiovascular Disorders (Mar 2023)

HOTAIR regulates SIRT3-mediated cardiomyocyte survival after myocardial ischemia/reperfusion by interacting with FUS

Jixuan Liu,
Mingzhuang Sun,
Jinda Wang,
Zhijun Sun,
Gang Wang

Affiliations

Jixuan Liu: Department of Cardiovascular, Beijing Friendship Hospital, Capital Medical University
Mingzhuang Sun: Department of Cardiovascular, Aerospace Central Hospital
Jinda Wang: Department of Cardiology, The Sixth Medical Centre of PLA General Hospital
Zhijun Sun: Department of Cardiology, The Sixth Medical Centre of PLA General Hospital
Gang Wang: Department of Cardiovascular, Beijing Friendship Hospital, Capital Medical University

DOI: https://doi.org/10.1186/s12872-023-03203-0
Journal volume & issue: Vol. 23, no. 1
pp. 1 – 12

Abstract

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Highlights 1. Overexpression of HOTAIR or SIRT3 promotes H/R-induced cardiomyocyte survival. 2. LncRNA HOTAIR regulates the expression of SIRT3 by binding to FUS. 3. HOTAIR/FUS/SIRT3 axis facilitates cardiomyocyte survival under H/R treatment.

Published in BMC Cardiovascular Disorders

ISSN: 1471-2261 (Online)
Publisher: BMC
Country of publisher: United Kingdom
LCC subjects: Medicine: Internal medicine: Specialties of internal medicine: Diseases of the circulatory (Cardiovascular) system
Website: https://bmccardiovascdisord.biomedcentral.com

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Abstract

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