ArticleCirculation research2011
Thioredoxin 1 negatively regulates angiotensin II-induced cardiac hypertrophy through upregulation of miR-98/let-7.
Article in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
74 citing papers in PubMed, 153 citations in OpenAlex.
- Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025Review
- Role of miRNAs in Regulating Ascending Aortic Dilation in Bicuspid Aortic Valve Patients Operated for Aortic Stenosis.International journal of molecular sciences · 2025Article
- Periodontal Tissue Homoeostasis, Immunity, the Red Complex Pathogens, and Dysbiosis: Unraveling the microRNA Effect.MicroRNA (Shariqah, United Arab Emirates) · 2025Review
- NADPCurrent medicinal chemistry · 2025Review
- Unique miRomics Expression Profiles inInternational journal of molecular sciences · 2023Article
- Article
- Characterization of the circulating transcriptome expression profile and identification of novel miRNA biomarkers in hypertrophic cardiomyopathy.European journal of medical research · 2023Article
- Targeting and delivery of microRNA-targeting antisense oligonucleotides in cardiovascular diseases.Atherosclerosis · 2023Review
- Thioredoxin 1 promotes autophagy through transnitrosylation of Atg7 during myocardial ischemia.The Journal of clinical investigation · 2023Article
- Change of Heart: the Epitranscriptome of Small Non-coding RNAs in Heart Failure.Current heart failure reports · 2022Review
- Long-Acting Thioredoxin Ameliorates Doxorubicin-Induced Cardiomyopathy via Its Anti-Oxidative and Anti-Inflammatory Action.Pharmaceutics · 2022Article
- Epitranscriptomics of cardiovascular diseases (Review).International journal of molecular medicine · 2022Review
- The Dynamic Role of NK Cells in Liver Cancers: Role in HCC and HBV Associated HCC and Its Therapeutic Implications.Frontiers in immunology · 2022Review
- The role and molecular mechanism of epigenetics in cardiac hypertrophy.Heart failure reviews · 2021Review
- Nampt Potentiates Antioxidant Defense in Diabetic Cardiomyopathy.Circulation research · 2021Article
- Simultaneous learning of individual microRNA-gene interactions and regulatory comodules.BMC bioinformatics · 2021Article
- The Impact of microRNAs in Renin-Angiotensin-System-Induced Cardiac Remodelling.International journal of molecular sciences · 2021Review
- Thioredoxin 1 (TRX1) Overexpression Cancels the Slow Force Response (SFR) Development.Frontiers in cardiovascular medicine · 2021Article
- Identification and Characterization of Circulating MicroRNAs as Novel Biomarkers in Dogs With Heart Diseases.Frontiers in veterinary science · 2021Article
- Expression Profile of Circulating MicroRNAs in Dogs With Cardiac Hypertrophy: A Pilot Study.Frontiers in veterinary science · 2021Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
rationaleThioredoxin (Trx)1 inhibits pathological cardiac hypertrophy. MicroRNAs (miRNAs) are small noncoding RNAs that downregulate posttranscriptional expression of target molecules.
objectivesWe investigated the role of miRNAs in mediating the antihypertrophic effect of Trx1 on angiotensin II (Ang II)-induced cardiac hypertrophy. METHODS AND
resultsMicroarray analyses of mature rodent microRNAs and quantitative RT-PCR/Northern blot analyses showed that Trx1 upregulates members of the let-7 family, including miR-98, in the heart and the cardiomyocytes therein. Adenovirus-mediated expression of miR-98 in cardiomyocytes reduced cell size both at baseline and in response to Ang II. Knockdown of miR-98, and of other members of the let-7 family, augmented Ang II-induced cardiac hypertrophy, and attenuated Trx1-mediated inhibition of Ang II-induced cardiac hypertrophy, suggesting that endogenous miR-98/let-7 mediates the antihypertrophic effect of Trx1. Cyclin D2 is one of the predicted targets of miR-98. Ang II significantly upregulated cyclin D2, which in turn plays an essential role in mediating Ang II-induced cardiac hypertrophy, whereas overexpression of Trx1 inhibited Ang II-induced upregulation of cyclin D2. miR-98 decreased both expression of cyclin D2 and the activity of a cyclin D2 3'UTR luciferase reporter, suggesting that both Trx1 and miR-98 negatively regulate cyclin D2. Overexpression of cyclin D2 attenuated the suppression of Ang II-induced cardiac hypertrophy by miR-98, suggesting that the antihypertrophic actions of miR-98 are mediated in part by downregulation of cyclin D2.
conclusionsThese results suggest that Trx1 upregulates expression of the let-7 family, including miR-98, which in turn inhibits cardiac hypertrophy, in part through downregulation of cyclin D2.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.