ArticleDiabetes2016
Lack of miR-133a Decreases Contractility of Diabetic Hearts: A Role for Novel Cross Talk Between Tyrosine Aminotransferase and Tyrosine Hydroxylase.
Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 55 citations in OpenAlex.
- A Systematic Bioinformatic Analysis of the miRNA Pathway in Inborn Errors of Amino Acid Metabolism Disorders.Molecular syndromology · 2026Article
- Biochemical study on microRNAs (miR-410, miR-133 and miR-582) in Egyptian type 1 diabetic patients.BMC endocrine disorders · 2025Article
- MicroRNAs in SARS-CoV-2 infection: emerging modulators of inflammation, pathogenesis, and therapeutic potential.Inflammopharmacology · 2025Review
- Pharmaceutical perspectives on oligonucleotide therapeutics and delivery systems.Pharmacological reviews · 2025Review
- Mechanistic insight into the role of cardiac-enriched microRNAs in diabetic heart injury.American journal of physiology. Heart and circulatory physiology · 2025Review
- QTL Mapping-Based Identification of Visceral White-Nodules Disease Resistance Genes inInternational journal of molecular sciences · 2024Article
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- Epigenetics in diabetic cardiomyopathy.Clinical epigenetics · 2024Review
- Deciphering MMP9's dual role in regulating SOD3 through protein-protein interactions.Canadian journal of physiology and pharmacology · 2024Article
- Primordial Drivers of Diabetes Heart Disease: Comprehensive Insights into Insulin Resistance.Diabetes & metabolism journal · 2024Review
- Enhanced central sympathetic tone induces heart failure with preserved ejection fraction (HFpEF) in rats.Frontiers in physiology · 2023Article
- Genome Editing and Diabetic Cardiomyopathy.Advances in experimental medicine and biology · 2023Article
- Article
- miR‑130b regulates PTEN to activate the PI3K/Akt signaling pathway and attenuate oxidative stress‑induced injury in diabetic encephalopathy.International journal of molecular medicine · 2021Article
- The Impact of microRNAs in Renin-Angiotensin-System-Induced Cardiac Remodelling.International journal of molecular sciences · 2021Review
- MicroRNAs and long non-coding RNAs in the pathophysiological processes of diabetic cardiomyopathy: emerging biomarkers and potential therapeutics.Cardiovascular diabetology · 2021Review
- Neurogenic Hypertension Mediated Mitochondrial Abnormality Leads to Cardiomyopathy: Contribution of UPRFrontiers in physiology · 2021Article
- Generating Ins2Methods in molecular biology (Clifton, N.J.) · 2021Article
- The Diabetic Cardiomyopathy: The Contributing Pathophysiological Mechanisms.Frontiers in medicine · 2021Review
- MMP9 inhibition increases autophagic flux in chronic heart failure.American journal of physiology. Heart and circulatory physiology · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
MicroRNAs (miRNAs) have a fundamental role in diabetic heart failure. The cardioprotective miRNA-133a (miR-133a) is downregulated, and contractility is decreased in diabetic hearts. Norepinephrine (NE) is a key catecholamine that stimulates contractility by activating β-adrenergic receptors (β-AR). NE is synthesized from tyrosine by the rate-limiting enzyme, tyrosine hydroxylase (TH), and tyrosine is catabolized by tyrosine aminotransferase (TAT). However, the cross talk/link between TAT and TH in the heart is unclear. To determine whether miR-133a plays a role in the cross talk between TH and TAT and regulates contractility by influencing NE biosynthesis and/or β-AR levels in diabetic hearts, Sprague-Dawley rats and miR-133a transgenic (miR-133aTg) mice were injected with streptozotocin to induce diabetes. The diabetic rats were then treated with miR-133a mimic or scrambled miRNA. Our results revealed that miR-133a mimic treatment improved the contractility of the diabetic rat's heart concomitant with upregulation of TH, cardiac NE, β-AR, and downregulation of TAT and plasma levels of NE. In miR-133aTg mice, cardiac-specific miR-133a overexpression prevented upregulation of TAT and suppression of TH in the heart after streptozotocin was administered. Moreover, miR-133a overexpression in CATH.a neuronal cells suppressed TAT with concomitant upregulation of TH, whereas knockdown and overexpression of TAT demonstrated that TAT inhibited TH. Luciferase reporter assay confirmed that miR-133a targets TAT. In conclusion, miR-133a controls the contractility of diabetic hearts by targeting TAT, regulating NE biosynthesis, and consequently, β-AR and cardiac function.
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