Circular RNA HMGCS1 sponges MIR4521 to aggravate type 2 diabetes-induced vascular endothelial dysfunction
Noncoding RNA plays a pivotal role as novel regulators of endothelial cell function. Type 2 diabetes, acknowledged as a primary contributor to cardiovascular diseases, plays a vital role in vascular endothelial cell dysfunction due to induced abnormalities of glucolipid metabolism and oxidative stre...
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Published in | eLife Vol. 13 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
England
eLife Sciences Publications Ltd
05.09.2024
eLife Sciences Publications, Ltd |
Subjects | |
Online Access | Get full text |
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Summary: | Noncoding RNA plays a pivotal role as novel regulators of endothelial cell function. Type 2 diabetes, acknowledged as a primary contributor to cardiovascular diseases, plays a vital role in vascular endothelial cell dysfunction due to induced abnormalities of glucolipid metabolism and oxidative stress. In this study, aberrant expression levels of
and
were observed in diabetes-induced human umbilical vein endothelial cell dysfunction. Persistent inhibition of
accelerated development and exacerbated vascular endothelial dysfunction in diabetic mice. Mechanistically,
upregulated arginase 1 by sponging
, leading to decrease in vascular nitric oxide secretion and inhibition of endothelial nitric oxide synthase activity, and an increase in the expression of adhesion molecules and generation of cellular reactive oxygen species, reduced vasodilation and accelerated the impairment of vascular endothelial function. Collectively, these findings illuminate the physiological role and interacting mechanisms of
and
in diabetes-induced cardiovascular diseases, suggesting that modulating the expression of
and
could serve as a potential strategy to prevent diabetes-associated cardiovascular diseases. Furthermore, our findings provide a novel technical avenue for unraveling ncRNAs regulatory roles of ncRNAs in diabetes and its associated complications. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 2050-084X 2050-084X |
DOI: | 10.7554/eLife.97267 |