ArticleJCI insight2016
CITED4 induces physiologic hypertrophy and promotes functional recovery after ischemic injury.
Article in JCI insight, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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.
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
60 citing papers in PubMed, 85 citations in OpenAlex.
- Age-dependent effects of aerobic training on cardiac expression of Akt1, mTOR, and CITED4 in immature, young-adult, and middle-aged rat myocardium.European journal of applied physiology · 2026Article
- Increasing cytosolic NADPH to mimic exercise.Nature metabolism · 2026Article
- Identification and analysis of EphrinB2/EphB4 signaling pathway and angiogenesis related biomarkers in coronary artery disease based on bioinformatics.Journal of cardiothoracic surgery · 2026Article
- Exercise-induced cardiac hypertrophy: cellular and molecular mechanisms of cardiac adaptation following physical activity.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2026Review
- MiR-199a family members are differentially regulated during physiological and pathological cardiac hypertrophy.Frontiers in physiology · 2026Article
- Macrophages lacking TSC2 have mTORC1-dependent increased GPNMB and ameliorate ventricular dysfunction/remodeling after ischemia-reperfusion.Scientific reports · 2025Article
- CITED Proteins in Cardiac Development and Lifelong Heart Function.Journal of personalized medicine · 2025Review
- Modeling myocardial physiological growth using human pluripotent stem cell derived cardiomyocytes and 3D cardiac microtissues.Cellular and molecular life sciences : CMLS · 2025Article
- Cited4a limits cardiomyocyte dedifferentiation and proliferation during zebrafish heart regeneration.Development (Cambridge, England) · 2025Article
- Cardiac ageing: from hallmarks to therapeutic opportunities.Cardiovascular research · 2025Review
- TargetingJournal of the American Heart Association · 2025Article
- Molecular Mediators of the Cardiac Benefits of Exercise.Circulation research · 2025Review
- Athlete's Heart Revisited: Historical, Clinical, and Molecular Perspectives.Circulation research · 2025Review
- CITED4 gene therapy protects against maladaptive cardiac remodeling after ischemia/reperfusion injury in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- CITED4 gene therapy: Can it be cited for preventing maladaptive post-ischemic cardiac remodeling?Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Cited2 is a key regulator of placental development and plasticity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Exercise-induced changes in myocardial glucose utilization during periods of active cardiac growth.Journal of molecular and cellular cardiology · 2024Article
- Intrinsic and Extrinsic Contributors to the Cardiac Benefits of Exercise.JACC. Basic to translational science · 2024Review
- Kv beta complex facilitates exercise-induced augmentation of myocardial perfusion and cardiac growth.Frontiers in cardiovascular medicine · 2024Article
- Exercise-Induced miR-210 Promotes Cardiomyocyte Proliferation and Survival and Mediates Exercise-Induced Cardiac Protection against Ischemia/Reperfusion Injury.Research (Washington, D.C.) · 2024Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The mechanisms by which exercise mediates its multiple cardiac benefits are only partly understood. Prior comprehensive analyses of the cardiac transcriptional components and microRNAs dynamically regulated by exercise suggest that the CBP/p300-interacting protein CITED4 is a downstream effector in both networks. While CITED4 has documented functional consequences in neonatal cardiomyocytes in vitro, nothing is known about its effects in the adult heart. To investigate the impact of cardiac CITED4 expression in adult animals, we generated transgenic mice with regulated, cardiomyocyte-specific CITED4 expression. Cardiac CITED4 expression in adult mice was sufficient to induce an increase in heart weight and cardiomyocyte size with normal systolic function, similar to the effects of endurance exercise training. After ischemia-reperfusion, CITED4 expression did not change initial infarct size but mediated substantial functional recovery while reducing ventricular dilation and fibrosis. Forced cardiac expression of CITED4 also induced robust activation of the mTORC1 pathway after ischemic injury. Moreover, pharmacological inhibition of mTORC1 abrogated CITED4's effects in vitro and in vivo. Together, these data establish CITED4 as a regulator of mTOR signaling that is sufficient to induce physiologic hypertrophy at baseline and mitigate adverse ventricular remodeling after ischemic injury.
Identifiers
What OpenQuestion 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 OpenQuestion graph.