Restoring diabetes-induced autophagic flux arrest in ischemic/reperfused heart by ADIPOR (adiponectin receptor) activation involves both AMPK-dependent and AMPK-independent signaling.

Authors

• Yajing Wang
• Bin Liang
• Wayne Bond Lau
• Yunhui Du
• Rui Guo
• Zheyi Yan
• Lu Gan
• Wenjun Yan
• Jianli Zhao
• Erhe Gao
• Walter Koch
• Xin-Liang Ma

Publication/Presentation Date

1-1-2017

Abstract

Macroautophagy/autophagy is increasingly recognized as an important regulator of myocardial ischemia-reperfusion (MI-R) injury. However, whether and how diabetes may alter autophagy in response to MI-R remains unknown. Deficiency of ADIPOQ, a cardioprotective molecule, markedly increases MI-R injury. However, the role of diabetic hypoadiponectinemia in cardiac autophagy alteration after MI-R is unclear. Utilizing normal control (NC), high-fat-diet-induced diabetes, and Adipoq knockout (adipoq

Volume

13

Issue

11

First Page

1855

Last Page

1869

ISSN

1554-8635

Published In/Presented At

Wang, Y., Liang, B., Lau, W. B., Du, Y., Guo, R., Yan, Z., Gan, L., Yan, W., Zhao, J., Gao, E., Koch, W., & Ma, X. L. (2017). Restoring diabetes-induced autophagic flux arrest in ischemic/reperfused heart by ADIPOR (adiponectin receptor) activation involves both AMPK-dependent and AMPK-independent signaling. Autophagy, 13(11), 1855–1869. https://doi.org/10.1080/15548627.2017.1358848

Disciplines

Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods

PubMedID

28825851

Department(s)

Administration and Leadership

Document Type

Article