Interleukin-1β, Oxidative Stress, and Abnormal Calcium Handling Mediate Diabetic Arrhythmic Risk

Hong Liu, Yang Zhao, An Xie, Tae Yun Kim, Radmila Terentyeva, Man Liu, Guangbin Shi, Feng Feng, Bum Rak Choi, Dmitry Terentyev, Shanna Hamilton, Samuel C. Dudley

Research output: Contribution to journalArticlepeer-review

28 Scopus citations


Diabetes mellitus (DM) is associated with increased arrhythmia. Type 2 DM (T2DM) mice showed prolonged QT interval and increased ventricular arrhythmic inducibility, accompanied by elevated cardiac interleukin (IL)-1β, increased mitochondrial reactive oxygen species (mitoROS), and oxidation of the sarcoplasmic reticulum (SR) Ca2+ release channel (ryanodine receptor 2 [RyR2]). Inhibiting IL-1β and mitoROS reduced RyR2 oxidation and the ventricular arrhythmia in DM. Inhibiting SR Ca2+ leak by stabilizing the oxidized RyR2 channel reversed the diabetic arrhythmic risk. In conclusion, cardiac IL-1β mediated the DM-associated arrhythmia through mitoROS generation that enhances SR Ca2+ leak. The mechanistic link between inflammation and arrhythmias provides new therapeutic options.

Original languageEnglish (US)
Pages (from-to)42-52
Number of pages11
JournalJACC: Basic to Translational Science
Issue number1
StatePublished - Jan 2021

Bibliographical note

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© 2021 The Authors


  • calcium handling
  • inflammation
  • mitochondria
  • oxidation
  • sudden cardiac death


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