ReviewCirculation research2018
New Myocyte Formation in the Adult Heart: Endogenous Sources and Therapeutic Implications.
Review in Circulation research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed.
- Multi-Omics Integration Reveals Incomplete Reactivation of Developmental Cell-Cycle Programs in Adult Human Infarcted Hearts.Chemical biology & drug design · 2026Article
- Inhibition of Scarb1 on Endothelial Cells Attenuates Pressure Overload-Induced Heart Failure Progression.JACC. Basic to translational science · 2025Article
- Stem Cell Therapy against Ischemic Heart Disease.International journal of molecular sciences · 2024Review
- IL-13 promotes functional recovery after myocardial infarction via direct signaling to macrophages.JCI insight · 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
- Growth factors and their roles in cardiac development and regeneration: a narrative review.Pediatric medicine (Hong Kong, China) · 2023Article
- Uncovering the Heterogeneity of Cardiac Lin-KIT+ Cells: A scRNA-seq Study on the Identification of Subpopulations.Stem cells (Dayton, Ohio) · 2023Article
- GDF11 and aging biology - controversies resolved and pending.The journal of cardiovascular aging · 2023Article
- Systemic Hypoxemia Induces Cardiomyocyte Hypertrophy and Right Ventricular Specific Induction of Proliferation.Circulation research · 2023Article
- Cre-loxP-mediated genetic lineage tracing: Unraveling cell fate and origin in the developing heart.Frontiers in cardiovascular medicine · 2023Review
- The ebb and flow of cardiac lymphatics: a tidal wave of new discoveries.Physiological reviews · 2023Review
- Wnt Signaling in Heart Development and Regeneration.Current cardiology reports · 2022Review
- Meta-Analysis of Percutaneous Endomyocardial Cell Therapy in Patients with Ischemic Heart Failure by Combination of Individual Patient Data (IPD) of ACCRUE and Publication-Based Aggregate Data.Journal of clinical medicine · 2022Article
- Clonal Tracing of Heart Regeneration.Journal of cardiovascular development and disease · 2022Review
- Cardiac Remodeling and Repair: Recent Approaches, Advancements, and Future Perspective.International journal of molecular sciences · 2021Review
- Targeting cardiomyocyte proliferation as a key approach of promoting heart repair after injury.Molecular biomedicine · 2021Review
- Biomimetic and immunomodulatory therapeutics as an alternative to natural exosomes for vascular and cardiac applications.Nanomedicine : nanotechnology, biology, and medicine · 2021Review
- Translation ofRNA biology · 2021Article
- Stem cell therapy for heart failure: Medical breakthrough, or dead end?World journal of stem cells · 2021Review
- Recapitulating Cardiac Structure and Function In Vitro from Simple to Complex Engineering.Micromachines · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Death of adult cardiac myocytes and supportive tissues resulting from cardiovascular diseases such as myocardial infarction is the proximal driver of pathological ventricular remodeling that often culminates in heart failure. Unfortunately, no currently available therapeutic barring heart transplantation can directly replenish myocytes lost from the injured heart. For decades, the field has struggled to define the intrinsic capacity and cellular sources for endogenous myocyte turnover in pursuing more innovative therapeutic strategies aimed at regenerating the injured heart. Although controversy persists to this day as to the best therapeutic regenerative strategy to use, a growing consensus has been reached that the very limited capacity for new myocyte formation in the adult mammalian heart is because of proliferation of existing cardiac myocytes but not because of the activity of an endogenous progenitor cell source of some sort. Hence, future therapeutic approaches should take into consideration the fundamental biology of myocyte renewal in designing strategies to potentially replenish these cells in the injured heart.
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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.