ReviewJournal of applied physiology (Bethesda, Md. : 1985)2017
Hypoxia-induced myocardial regeneration.
Review in Journal of applied physiology (Bethesda, Md. : 1985), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 45 citations in OpenAlex.
- Oxygen physiology and mechanisms of oxygen toxicity: a narrative review.Medical gas research · 2026Review
- Hypoxia Increases Cardiac Proteasomal Activity and Differentially Modulates Cullin-RING E3 Ligases in the Naked Mole-RatMuscles (Basel, Switzerland) · 2026Article
- Migration of Cardiac Cells: Hot Topics that have not Attracted Clinical Attention.International journal of medical sciences · 2026Review
- Review
- Review
- A Latent Cardiomyocyte Regeneration Potential in Human Heart Disease.Circulation · 2025Article
- A hypoxia-on-a-chip platform for modeling ischemic arrhythmogenesis and evaluating the effects of levosimendan and OR-1896 on ischemic human iPSC-derived cardiomyocytes.Frontiers in bioengineering and biotechnology · 2025Article
- Hypoxia-responsive zinc finger E-box-binding homeobox 2 (ZEB2) regulates a network of calcium-handling genes in the injured heart.Cardiovascular research · 2024Article
- Regenerative loss in the animal kingdom as viewed from the mouse digit tip and heart.Developmental biology · 2024Review
- Hypoxia Attenuates Pressure Overload-Induced Heart Failure.Journal of the American Heart Association · 2024Article
- MDM2 Regulation of HIF Signaling Causes Microvascular Dysfunction in Hypertrophic Cardiomyopathy.Circulation · 2023Article
- Diversity of cells and signals in the cardiovascular system.The Journal of physiology · 2023Article
- New treatment methods for myocardial infarction.Frontiers in cardiovascular medicine · 2023Review
- Regulation of extracellular matrix composition by fibroblasts during perinatal cardiac maturation.Journal of molecular and cellular cardiology · 2022Article
- Cardiomyocyte Proliferation from Fetal- to Adult- and from Normal- to Hypertrophy and Failing Hearts.Biology · 2022Review
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- Cell-Based HIF1α Gene Therapy Reduces Myocardial Scar and Enhances Angiopoietic Proteome, Transcriptomic and miRNA Expression in Experimental Chronic Left Ventricular Dysfunction.Frontiers in bioengineering and biotechnology · 2022Article
- Innate Mechanisms of Heart Regeneration.Cold Spring Harbor perspectives in biology · 2021Review
- Human Engineered Heart Tissue Patches Remuscularize the Injured Heart in a Dose-Dependent Manner.Circulation · 2021Article
- Reactive oxygen species during heart regeneration in zebrafish: Lessons for future clinical therapies.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 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 at 1 institution in 2 countries.
Funding
Abstract
The underlying cause of systolic heart failure is the inability of the adult mammalian heart to regenerate damaged myocardium. In contrast, some vertebrate species and immature mammals are capable of full cardiac regeneration following multiple types of injury through cardiomyocyte proliferation. Little is known about what distinguishes proliferative cardiomyocytes from terminally differentiated, nonproliferative cardiomyocytes. Recently, several reports have suggested that oxygen metabolism and oxidative stress play a pivotal role in regulating the proliferative capacity of mammalian cardiomyocytes. Moreover, reducing oxygen metabolism in the adult mammalian heart can induce cardiomyocyte cell cycle reentry through blunting oxidative damage, which is sufficient for functional improvement following myocardial infarction. Here we concisely summarize recent findings that highlight the role of oxygen metabolism and oxidative stress in cardiomyocyte cell cycle regulation, and discuss future therapeutic approaches targeting oxidative metabolism to induce cardiac regeneration.
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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.