ArticleCell reports2016
Integrative Analysis of PRKAG2 Cardiomyopathy iPS and Microtissue Models Identifies AMPK as a Regulator of Metabolism, Survival, and Fibrosis.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 55 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
55 citing papers in PubMed, 94 citations in OpenAlex.
- AMPKγ2 Meets Myosin: A New Link Between Metabolism and Sarcomere Function.Circulation research · 2026Article
- AMPKγ2 Regulates Cardiac Hypertrophy and Arrhythmias via Interacting With Myosin.Circulation research · 2026Article
- Advanced in vitro cardiac models for drug evaluation: integration of organoids, engineered tissues, and microphysiological systems.Microsystems & nanoengineering · 2026Review
- PRKAG2 Cardiomyopathy: A Case-Control Study on the Diagnostic Yield Of Histopathology and Ultrastructural Analysis from Endomyocardial Biopsy.Arquivos brasileiros de cardiologia · 2026Observational
- Bioenergetic and metabolic aberrations in induced pluripotent stem cell-derived cardiomyocytes generated from a patient with Wolff-Parkinson-White syndrome caused aFrontiers in cardiovascular medicine · 2026Article
- Human Cardiac Organoids: Advances and Prospects from Construction to Preclinical Drug Evaluation.Cells · 2025Review
- Temporal dysregulation ofResearch square · 2025Article
- Three-dimensional cardiac models: a pre-clinical testing platform.Biochemical Society transactions · 2024Review
- Role and molecular mechanisms of SGLT2 inhibitors in pathological cardiac remodeling (Review).Molecular medicine reports · 2024Review
- Article
- AMPK activator-treated human cardiac spheres enhance maturation and enable pathological modeling.Stem cell research & therapy · 2023Article
- Modeling and countering the effects of cosmic radiation using bioengineered human tissues.Biomaterials · 2023Article
- Analysis of cardiac single-cell RNA-sequencing data can be improved by the use of artificial-intelligence-based tools.Scientific reports · 2023Article
- Cardiomyocyte infection byFrontiers in cellular and infection microbiology · 2023Article
- PRKAG2 Cardiomyopathy.Arquivos brasileiros de cardiologia · 2022Article
- Characterization of cardiac metabolism in iPSC-derived cardiomyocytes: lessons from maturation and disease modeling.Stem cell research & therapy · 2022Review
- Controversial molecular functions of CBS versus non-CBS domain variants of PRKAG2 in arrhythmia and cardiomyopathy: A case report and literature review.Molecular genetics & genomic medicine · 2022Review
- Reading Frame Repair ofCirculation · 2022Article
- Human Engineered Heart Tissue Models for Disease Modeling and Drug Discovery.Frontiers in cell and developmental biology · 2022Review
- 3D models of dilated cardiomyopathy: Shaping the chemical, physical and topographical properties of biomaterials to mimic the cardiac extracellular matrix.Bioactive materials · 2022Review
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 8 institutions in 1 country.
Funding
Abstract
AMP-activated protein kinase (AMPK) is a metabolic enzyme that can be activated by nutrient stress or genetic mutations. Missense mutations in the regulatory subunit, PRKAG2, activate AMPK and cause left ventricular hypertrophy, glycogen accumulation, and ventricular pre-excitation. Using human iPS cell models combined with three-dimensional cardiac microtissues, we show that activating PRKAG2 mutations increase microtissue twitch force by enhancing myocyte survival. Integrating RNA sequencing with metabolomics, PRKAG2 mutations that activate AMPK remodeled global metabolism by regulating RNA transcripts to favor glycogen storage and oxidative metabolism instead of glycolysis. As in patients with PRKAG2 cardiomyopathy, iPS cell and mouse models are protected from cardiac fibrosis, and we define a crosstalk between AMPK and post-transcriptional regulation of TGFβ isoform signaling that has implications in fibrotic forms of cardiomyopathy. Our results establish critical connections among metabolic sensing, myocyte survival, and TGFβ signaling.
Indexed as
Identifiers
What Socratic holds
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.