Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 7, Pages -Publisher
MDPI
DOI: 10.3390/ijms22073796
Keywords
sphingolipids; stroke; brain; kidney; SHR; WKY
Funding
- Italian Ministry of Health
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The study found abnormalities in sphingolipid metabolism in the brains and kidneys of hypertensive rats, particularly more noticeable in the stroke-prone rats. These findings suggest that defects in specific lipid molecules and metabolic pathways may contribute to the pathogenesis of hypertensive target organ damage. Further research is needed to fully understand the significance of these findings and their potential as therapeutic targets for reducing vascular consequences of hypertension.
Alterations in the metabolism of sphingolipids, a class of biologically active molecules in cell membranes with direct effect on vascular homeostasis, are increasingly recognized as important determinant in different vascular disorders. However, it is not clear whether sphingolipids are implicated in the pathogenesis of hypertension-related cerebrovascular and renal damage. In this study, we evaluated the existence of possible abnormalities related to the sphingolipid metabolism in the brain and kidneys of two well validated spontaneously hypertensive rat strains, the stroke-prone (SHRSP) and the stroke-resistant (SHRSR) models, as compared to the normotensive Wistar Kyoto (WKY) rat strain. Our results showed a global alteration in the metabolism of sphingolipids in both cerebral and renal tissues of both hypertensive strains as compared to the normotensive rat. However, few defects, such as reduced expression of enzymes involved in the metabolism/catabolism of sphingosine-1-phosphate and in the de novo biosynthetic pathways, were exclusively detected in the SHRSP. Although further studies are necessary to fully understand the significance of these findings, they suggest that defects in specific lipid molecules and/or their related metabolic pathways may likely contribute to the pathogenesis of hypertensive target organ damage and may eventually serve as future therapeutic targets to reduce the vascular consequences of hypertension.
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