ArticleAmerican journal of physiology. Heart and circulatory physiology2009
Apoptosis predominates in nonmyocytes in heart failure.
Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- The Role of microRNAs in Heart Failure: A Systematic Review.Frontiers in cardiovascular medicine · 2020Pooled it
- Levosimendan reduces plasma cell-free DNA levels in patients with ischemic cardiomyopathy.Journal of thrombosis and thrombolysis · 2011Trial
- Machine Learning Integrates Bulk and Single-Nucleus RNA Sequence to Explore Apoptosis-Related Gene in Myocardial Infarction.Cardiovascular therapeutics · 2026Article
- Role and mechanism of miRNA in cardiac microvascular endothelial cells in cardiovascular diseases.Frontiers in cardiovascular medicine · 2024Review
- Advances in the study of exosomes derived from mesenchymal stem cells and cardiac cells for the treatment of myocardial infarction.Cell communication and signaling : CCS · 2023Review
- The phagocytic role of macrophage following myocardial infarction.Heart failure reviews · 2023Review
- Cardiomyocytes disrupt pyrimidine biosynthesis in nonmyocytes to regulate heart repair.The Journal of clinical investigation · 2022Article
- Interplay of Oxidative Stress and Necrosis-like Cell Death in Cardiac Ischemia/Reperfusion Injury: A Focus on Necroptosis.Biomedicines · 2022Review
- Programmed Cell Death of Endothelial Cells in Myocardial Infarction and Its Potential Therapeutic Strategy.Cardiology research and practice · 2022Review
- The Networks of Noncoding RNAs and Their Direct Molecular Targets in Myocardial Infarction.International journal of biological sciences · 2022Review
- Pharmacology of Catechins in Ischemia-Reperfusion Injury of the Heart.Antioxidants (Basel, Switzerland) · 2021Review
- Cardiac telocytes inhibit cardiac microvascular endothelial cell apoptosis through exosomal miRNA-21-5p-targetedTheranostics · 2021Article
- Serelaxin alleviates cardiac fibrosis through inhibiting endothelial-to-mesenchymal transition via RXFP1.Theranostics · 2020Article
- Autophagy and Oncosis/Necroptosis Are Enhanced in Cardiomyocytes from Heart Failure Patients.Medical science monitor basic research · 2019Article
- Three in a Box: Understanding Cardiomyocyte, Fibroblast, and Innate Immune Cell Interactions to Orchestrate Cardiac Repair Processes.Frontiers in cardiovascular medicine · 2019Review
- Angiogenic Endothelial Cell Signaling in Cardiac Hypertrophy and Heart Failure.Frontiers in cardiovascular medicine · 2019Review
- Anti-apoptosis in nonmyocytes and pro-autophagy in cardiomyocytes: two strategies against postinfarction heart failure through regulation of cell death/degeneration.Heart failure reviews · 2018Review
- Truncations of the titin Z-disc predispose to a heart failure with preserved ejection phenotype in the context of pressure overload.PloS one · 2018Article
- Mechanisms and Therapeutic Targets of Cardiac Regeneration: Closing the Age Gap.Frontiers in cardiovascular medicine · 2018Review
- Analysis of necroptotic proteins in failing human hearts.Journal of translational medicine · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
The goal of this investigation was to determine the distribution of myocardial apoptosis in myocytes and nonmyocytes in primates and patients with heart failure (HF). Almost all clinical cardiologists and cardiovascular investigators believe that myocyte apoptosis is considered to be a cardinal sign of HF and a major factor in its pathogenesis. However, with the knowledge that 75% of the number of cells in the heart are nonmyocytes, it is important to determine whether the apoptosis in HF is occurring in myocytes or in nonmyocytes. We studied both a nonhuman primate model of chronic HF, induced by rapid pacing 2-6 mo after myocardial infarction (MI), and biopsies from patients with ischemic cardiomyopathy. Dual labeling with a cardiac muscle marker was used to discriminate apoptosis in myocytes versus nonmyocytes. Left ventricular ejection fraction decreased following MI (from 78% to 60%) and further with HF (35%, P < 0.05). As expected, total apoptosis was increased in the myocardium following recovery from MI (0.62 cells/mm(2)) and increased further with the development of HF (1.91 cells/mm(2)). Surprisingly, the majority of apoptotic cells in MI and MI + HF, and in both the adjacent and remote areas, were nonmyocytes. This was also observed in myocardial biopsies from patients with ischemic cardiomyopathy. We found that macrophages contributed the largest fraction of apoptotic nonmyocytes (41% vs. 18% neutrophils, 16% fibroblast, and 25% endothelial and other cells). Although HF in the failing human and monkey heart is characterized by significant apoptosis, in contrast to current concepts, the apoptosis in nonmyocytes was eight- to ninefold greater than in myocytes.
Indexed as
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.