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In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
Published on: October 27, 2020
Autophagy induced by ischemic preconditioning is essential for cardioprotection
Chengqun Huang1, Smadar Yitzhaki, Cynthia N Perry
1BioScience Center, San Diego State University, 5500 Campanile Drive, San Diego, CA 92182-4650, USA.
Journal of Cardiovascular Translational Research
|June 19, 2010
Summary
Autophagy is essential for heart protection during ischemic preconditioning (IPC). Inhibiting autophagy significantly reduced cardioprotection, confirming its role in both ischemic and pharmacologic preconditioning.
Area of Science:
- Cardiovascular Biology
- Cellular Mechanisms
- Autophagy Research
Background:
- Growing evidence suggests a link between autophagy and preconditioning.
- The precise role of autophagy in ischemic preconditioning (IPC) remains to be fully elucidated.
Purpose of the Study:
- To test the hypothesis that autophagy is necessary for cardioprotection conferred by IPC.
- To investigate the role of autophagy in pharmacologic preconditioning.
Main Methods:
- IPC was induced in mice and Langendorff-perfused hearts.
- Autophagy was assessed using mCherry-LC3 transgenic mice, Western blotting, and cadaverine dye binding.
- Autophagy was inhibited using Tat-ATG5(K130R) to evaluate its role in cardioprotection.
Main Results:
- IPC rapidly increased autophagosome formation in preconditioned hearts.
- Inhibition of autophagy with Tat-ATG5(K130R) reduced IPC-mediated cardioprotection.
- Three unrelated cardioprotective agents (UTP, diazoxide, ranolazine) induced autophagy, and its inhibition abolished their protective effects.
Conclusions:
- Autophagy is a necessary component of cardioprotection induced by ischemic preconditioning.
- Autophagy acts as an end-effector in both ischemic and pharmacologic preconditioning.
- These findings highlight autophagy as a therapeutic target for cardiac protection.
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