ReviewPhysiological reviews2019
Fundamental Mechanisms of Regulated Cell Death and Implications for Heart Disease.
Review in Physiological reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 555 papers, 1 of them a synthesis that pooled it.
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
555 citing papers in PubMed, 1 synthesis or guideline pooled it, 918 citations in OpenAlex.
- Pooled it
- Changes in Circulating Biomarkers in Patients With Ischemic Heart Failure After Treatment With Autologous Mesenchymal Stromal Cells and c-Kit-Positive Cardiac Cells, Alone or in Combination: Results From the Cardiovascular Cell Therapy Research Network CONCERT-HF Clinical Trial.Journal of the American Heart Association · 2026Trial
- Circadian mechanisms in heart failure: Cell-specific regulation and chrono-medicine.Cell insight · 2026Review
- Targeting integrated cell death networks in sepsis‑associated acute kidney injury: Shared regulatory nodes and diet‑related small molecule modulation (Review).International journal of molecular medicine · 2026Review
- METTL3 Confers Ischemia/Reperfusion-Caused Myocardial Injury by Triggering Ferroptosis via Regulating the lncRNA SNHG14/miR-195a-5p/ACSL4 Axis.Cardiovascular drugs and therapy · 2026Article
- Targeting efferocytosis with carbonized polymer dots from a natural anti-inflammatory drug to alleviate excessive inflammatory responses in the acute phase of myocardial infarction.Materials today. Bio · 2026Article
- Imbalance of the Regulated Cell Death and Autophagic Network: A Core Mechanism Driving Toxicological and Ischemic Myocardial Injury and a Target for Intervention with Traditional Chinese Medicine.Cardiovascular toxicology · 2026Review
- Deciphering the rules of regulated cell death subroutines by in silico methods.Journal of advanced research · 2026Review
- Role of PANoptosis in the development of gastric immunity and related gastric mucosal disease (Review).Molecular medicine reports · 2026Review
- Mechanisms underlying propagation of ferroptotic cell death.Nature cell biology · 2026Review
- An enantioselective covalent inhibitor of BAX confers cytoprotection in vivo.Nature chemical biology · 2026Article
- A safety pin against BAX.Nature chemical biology · 2026Article
- Programmed cell death in adenomyosis: mechanisms and future perspectives.Molecular biology reports · 2026Review
- Mechanisms and Translational Potential of Plant-Derived Extracellular Vesicles in Cardiovascular Disease.Cells · 2026Review
- Brown Adipocyte Sheets Alleviate Myocardial Ischemia-Reperfusion Injury Through NRG4-ErbB4-Dependent Ferroptosis Inhibition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Dying for Clarity: Common Pitfalls in Cardiac Cell Death Research.Cardiovascular drugs and therapy · 2026Article
- Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia-reperfusion injury.The Journal of physiology · 2026Review
- Polarized Light Microscopy for Quantitative Assessment of Sarcomere-Scale Structural Order in Cardiac Tissue.Journal of biophotonics · 2026Article
- FGF21-FGFR1 signaling protects against cardiac hypertrophy by regulating PINK1-mediated mitophagy pathway.Journal of advanced research · 2026Article
- Necroptosis in alveolar epithelium orchestrates lung ischemia-reperfusion injury: a multi-omics study.Respiratory research · 2026Article
495 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Twelve regulated cell death programs have been described. We review in detail the basic biology of nine including death receptor-mediated apoptosis, death receptor-mediated necrosis (necroptosis), mitochondrial-mediated apoptosis, mitochondrial-mediated necrosis, autophagy-dependent cell death, ferroptosis, pyroptosis, parthanatos, and immunogenic cell death. This is followed by a dissection of the roles of these cell death programs in the major cardiac syndromes: myocardial infarction and heart failure. The most important conclusion relevant to heart disease is that regulated forms of cardiomyocyte death play important roles in both myocardial infarction with reperfusion (ischemia/reperfusion) and heart failure. While a role for apoptosis in ischemia/reperfusion cannot be excluded, regulated forms of necrosis, through both death receptor and mitochondrial pathways, are critical. Ferroptosis and parthanatos are also likely important in ischemia/reperfusion, although it is unclear if these entities are functioning as independent death programs or as amplification mechanisms for necrotic cell death. Pyroptosis may also contribute to ischemia/reperfusion injury, but potentially through effects in non-cardiomyocytes. Cardiomyocyte loss through apoptosis and necrosis is also an important component in the pathogenesis of heart failure and is mediated by both death receptor and mitochondrial signaling. Roles for immunogenic cell death in cardiac disease remain to be defined but merit study in this era of immune checkpoint cancer therapy. Biology-based approaches to inhibit cell death in the various cardiac syndromes are also discussed.
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.