Abstract
Liver-X-receptor (LXR) has previously been shown to exert a cardioprotective effect against the development of diabetic cardiomyopathy (DCM) associated with a reduction in mitochondrial dysfunction. However, the underlying mechanism by which LXR activation attenuates the structural and functional mitochondrial impairments caused by high glucose (HG) stress remains unclear. We demonstrate here that LXR activation inhibits HG stress-induced mitochondrial dysfunction and ameliorates aberrant mitochondrial dynamics. Furthermore, LXR activation regulates mitochondrial dynamics by inhibiting HG stress-induced upregulation of Calpain1 expression. These data indicate that amelioration of Calpain1-mediated aberrant mitochondrial dynamics may be at least part of the mechanism underlying the cardioprotective effects of LXR against HG stress. Therefore, LXR is a potentially attractive molecular target for treating cardiac mitochondrial dysfunction in patients with diabetes.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Biochemical and Biophysical Research Communications
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
