ArticleBioengineered2021
miR-337-5p promotes the development of cardiac hypertrophy by targeting Ubiquilin-1 (UBQLN1).
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- MiR-107 as a Biomarker Predicts Cardiac Hypertrophy in Chronic Hemodialysis Patients.Anatolian journal of cardiology · 2025Article
- Sertraline-induced 5-HT dysregulation in mouse cardiomyocytes and the impact on calcium handling.American journal of physiology. Heart and circulatory physiology · 2024Article
- Autophagy and mitophagy as potential therapeutic targets in diabetic heart condition: Harnessing the power of nanotheranostics.Asian journal of pharmaceutical sciences · 2024Review
- Sacubitril/valsartan (LCZ696) ameliorates hyperthyroid-induced cardiac hypertrophy in male rats through modulation of miR-377, let-7 b, autophagy, and fibrotic signaling pathways.Scientific reports · 2022Article
- Article
- MiR-410-3p facilitates Angiotensin II-induced cardiac hypertrophy by targeting Smad7.Bioengineered · 2022Article
- Upregulation of miR-140-5p uncouples mitochondria by targeting Bcl-xL in vascular smooth muscle cells in angiotensin II-induced hypertension.Bioengineered · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is an adaptive response of the myocardium to the pressure overload of the heart. MicroRNAs (miRNAs/miRs) are shown to be directly involved in the development of cardiac hypertrophy. However, the function of miR-337-5p and its potential contribution to the serine/threonine-protein kinase, a mammalian target of rapamycin (mTOR) signaling in cardiac hypertrophy remains unknown. In the present study, miR-337-5p expression was examined in cardiomyocytes treated with angiotensin II (Ang II). An adenovirus vector system was employed to knockdown miR-337-5p expression to investigate its functions in cardiac hypertrophy. The results revealed a significant increase in the expression of miR-337-5p in cardiomyocytes treated with Ang II as compared with controls. In addition, downregulation of miR-337-5p expression inhibited cardiac hypertrophy both
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