ArticleThe Journal of clinical investigation2017
Cardiomyocyte proliferation prevents failure in pressure overload but not volume overload.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 44 citations in OpenAlex.
- PCPE-1 promotes cardiac fibrosis with aging and obesity.JCI insight · 2026Article
- Insights into Cardiomyocyte Regeneration from Screening and Transcriptomics Approaches.International journal of molecular sciences · 2026Review
- Article
- Cardioprotective strategies in myocardial ischemia-reperfusion injury: Implications for improving clinical translation.Journal of molecular and cellular cardiology plus · 2025Review
- Microparticle Mediated Delivery of Apelin Improves Heart Function in Post Myocardial Infarction Mice.Circulation research · 2024Article
- STEMIN and YAP5SA, the future of heart repair?Experimental biology and medicine (Maywood, N.J.) · 2024Review
- Effects of maternal hypothyroidism on postnatal cardiomyocyte proliferation and cardiac disease responses of the progeny.American journal of physiology. Heart and circulatory physiology · 2023Article
- Musings on intrinsic cardiomyocyte cell cycle activity and myocardial regeneration.Journal of molecular and cellular cardiology · 2023Review
- Regulation of endogenous cardiomyocyte proliferation: The known unknowns.Journal of molecular and cellular cardiology · 2023Review
- Proteomic Analysis in Valvular Cardiomyopathy: Aortic Regurgitation vs. Aortic Stenosis.Cells · 2023Article
- LncRNA AC005332.7 Inhibited Ferroptosis to Alleviate Acute Myocardial Infarction Through Regulating miR-331-3p/CCND2 Axis.Korean circulation journal · 2023Article
- The Role of Long Non-Coding RNA (LncRNA) in Acute Myocardial Infarction: Novel Strategy for the Treatment of Acute Myocardial Infarction.Korean circulation journal · 2023Article
- Cardiac Troponin I-Interacting Kinase Affects Cardiomyocyte S-Phase Activity but Not Cardiomyocyte Proliferation.Circulation · 2023Article
- Ability of the Right Ventricle to Serve as a Systemic Ventricle in Response to the Volume Overload at the Neonatal Stage.Biology · 2022Article
- Turning back the clock: A concise viewpoint of cardiomyocyte cell cycle activation for myocardial regeneration and repair.Journal of molecular and cellular cardiology · 2022Review
- Article
- Analysis of myocardial cellular gene expression during pressure overload reveals matrix based functional intercellular communication.iScience · 2022Article
- Cardiomyocyte Proliferation as a Source of New Myocyte Development in the Adult Heart.International journal of molecular sciences · 2021Review
- Mechanisms Underlying Cardiomyocyte Development: Can We Exploit Them to Regenerate the Heart?Current cardiology reports · 2021Review
- I-Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Induction of the cell cycle is emerging as an intervention to treat heart failure. Here, we tested the hypothesis that enhanced cardiomyocyte renewal in transgenic mice expressing cyclin D2 would be beneficial during hemodynamic overload. We induced pressure overload by transthoracic aortic constriction (TAC) or volume overload by aortocaval shunt in cyclin D2-expressing and WT mice. Although cyclin D2 expression dramatically improved survival following TAC, it did not confer a survival advantage to mice following aortocaval shunt. Cardiac function decreased following TAC in WT mice, but was preserved in cyclin D2-expressing mice. On the other hand, cardiac structure and function were compromised in response to aortocaval shunt in both WT and cyclin D2-expressing mice. The preserved function and improved survival in cyclin D2-expressing mice after TAC was associated with an approximately 50% increase in cardiomyocyte number and exaggerated cardiac hypertrophy, as indicated by increased septum thickness. Aortocaval shunt did not further impact cardiomyocyte number in mice expressing cyclin D2. Following TAC, cyclin D2 expression attenuated cardiomyocyte hypertrophy, reduced cardiomyocyte apoptosis, fibrosis, calcium/calmodulin-dependent protein kinase IIδ phosphorylation, brain natriuretic peptide expression, and sustained capillarization. Thus, we show that cyclin D2-induced cardiomyocyte renewal reduced myocardial remodeling and dysfunction after pressure overload but not after volume overload.
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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.