This article [Ognjen Culic et al., 1999: (http://ajpcell.physiology.org/cgi/content/full/276/5/C1061) (http://www.ncbi.nlm.nih.gov/pubmed/10329953)] is interesting, and the authors discuss the reliance of endothelial cells on triglycerides for fuel. That's really interesting and may be relevant to understanding the association of low cholesterol and hemorrhagic stroke, for example. Some researchers have explained that association in terms of the capacity of an increase in the cellular cholesterol content to reduce the sensitivity of smooth muscle cells to anoxia. Cholesterol is degraded via the propionate pathway (it can be) and could be anaplerotic in that regard, but these articles on endothelial cells' reliance on glycolysis suggest that glycolytic ATP production in endothelial cells and not just smooth muscle cells could be important for preventing hemorrhages. Most of the research on mechanisms of hemorrhage is in relation to arterial hemorrhages in the context of hypertension, with the arterionecrosis, or smooth muscle cell necrosis, setting the stage, so to speak, for the reperfusion-induced hemorrhage. But for the prevention of venous hemorrhages, maintaining ATP production in endothelial cells might be an important factor.
That article also discusses the large contribution that endothelial cells make to de novo purine biosynthesis for the heart as a whole, and the authors discuss the high rate of turnover of purines in endothelial cells.
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