- Poster presentation
- Open Access
Endothelial dysfunction in a mouse model of human neutral lipid storage disease
© Schrammel et al; licensee BioMed Central Ltd. 2013
- Published: 29 August 2013
- Endothelial Dysfunction
- Proteasomal Activity
- Triglyceride Lipase
- eNOS Protein
Systemic knockout of adipose triglyceride lipase (ATGL), the rate-limiting enzyme of triglyceride catabolism, results in a murine phenotype characterized by progressive accumulation of lipids in the heart finally leading to lethal cardiac dysfunction. Since cardiac and vascular dysfunction are closely related we investigated endothelium-dependent and -independent vessel function of ATGL knockout (ATGL(-/-)) mice. Using mice with cardiomyocyte-restricted overexpression of ATGL (cardiac-rescued phenotype;
ATGL(-/-)/MHC-A35) we were able to differentiate between heart-related and -unrelated effects.
Endothelial dysfunction in murine ATGL deficiency partly arises from impaired cardiac contractility and originates from down-regulation of aortic eNOS presumably due to activation of the vascular proteasome. Potential heart-independent mechanisms contributing to the observed defect are currently investigated.
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.