Key result
Delivery of miR-101a mimics significantly suppressed hypoxia-induced expression of TGFβRI and p-Smad 3, cardiac fibroblast differentiation, and collagen content.
Population
Rats with coronary artery occlusion and cultured rat neonatal cardiac fibroblasts exposed to hypoxia.
Comparison
Delivery of miR-101a mimics vs Hypoxia alone or co-transfection with AMO-miR-101a
Design
Preclinical
Follow-up
2 weeks (in vivo model)
Authors
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Supports miR-101a as anti-fibrotic target in fibroblasts; hypothesis-generating for post-infarct remodeling therapies.
miR-101a exerts anti-fibrotic effects in hypoxic cardiac fibroblasts by targeting TGFβRI, highlighting its potential role in mitigating post-infarct cardiac remodeling.
Zhao et al. (2015) studied Cardiac fibrosis. miR-101a mimics vs. Hypoxia control / AMO-miR-101a was evaluated on Expression of TGFβRI, p-Smad 3, CF differentiation, and collagen content. Delivery of miR-101a mimics significantly suppressed hypoxia-induced expression of TGFβRI and p-Smad 3, cardiac fibroblast differentiation, and collagen content.
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