Key result
lncRNA-MIAT promotes cell viability and inhibits apoptosis in human aortic vascular smooth muscle cells by targeting miR-145 and regulating the PI3K/Akt signaling pathway.
Why the study?
The study aimed to investigate the roles and molecular basis of long noncoding RNA myocardial infarction associated transcript (MIAT) in the development of thoracic aortic aneurysm.
Population
Thoracic aortic aneurysm tissues, normal thoracic aortic tissues, and human aortic vascular smooth muscle cells
Comparison
MIAT modulation, miR-145 modulation, and Akt pathway inhibition or activation
Design
Preclinical laboratory study
Authors
Loading...
Supports lncRNA-MIAT as a target in aneurysm models; leaves open clinical translation from cell data.
lncRNA-MIAT promotes thoracic aortic aneurysm development by enhancing vascular smooth muscle cell viability and reducing apoptosis through the miR-145/PI3K/Akt axis.
Chen et al. (2019) studied Thoracic aortic aneurysm. MIAT overexpression and miR-145 depletion vs. Normal thoracic aortic tissues and control cells was evaluated on Cell viability and apoptosis. lncRNA-MIAT promotes cell viability and inhibits apoptosis in human aortic vascular smooth muscle cells by targeting miR-145 and regulating the PI3K/Akt signaling pathway.
Synapse has enriched 2 closely related papers on similar clinical questions. Consider them for comparative context: