ReviewInternational journal of cardiology. Heart & vasculature2023
How does NFAT3 regulate the occurrence of cardiac hypertrophy?
Review in International journal of cardiology. Heart & vasculature, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 2 citations in OpenAlex.
- A Seven Amino Acid Long Region in the Cardiac CaCells · 2026Article
- The ADP-ribosyltransferases 3 (ART3) is a novel suppressor of pathological cardiac hypertrophy by ribosylating ITGA7.Acta pharmaceutica Sinica. B · 2026Article
- Anti-Atherogenic Actions of Pomegranate Polyphenol Punicalagin and Its Metabolites: In Vitro Effects on Vascular Cells and In Vivo Atheroprotection by Urolithin A via Anti-Inflammatory and Plaque-Stabilising Mechanisms.Antioxidants (Basel, Switzerland) · 2026Article
- Transcriptional regulation in cardiovascular aging.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac hypertrophy is initially an adaptive response to physiological and pathological stimuli. Although pathological myocardial hypertrophy is the main cause of morbidity and mortality, our understanding of its mechanism is still weak. NFAT3 (nuclear factor of activated T-cell-3) is a member of the nuclear factor of the activated T cells (NFAT) family. NFAT3 plays a critical role in regulating the expression of cardiac hypertrophy genes by inducing their transcription. Recently, accumulating evidence has indicated that NFAT3 is a potent regulator of the progression of cardiac hypertrophy. This review, for the first time, summarizes the current studies on NFAT3 in cardiac hypertrophy, including the pathophysiological processes and the underlying pathological mechanism, focusing on the nuclear translocation and transcriptional function of NFAT3. This review will provide deep insight into the pathogenesis of cardiac hypertrophy and a theoretical basis for identifying new therapeutic targets in the NFAT3 network.
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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 Socratic graph.