ReviewHeart failure reviews2016
Necroptotic cell death in failing heart: relevance and proposed mechanisms.
Review in Heart failure reviews, 2016. 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
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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
41 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection.Basic research in cardiology · 2018Guideline
- Global research trends of cell death in diabetic cardiomyopathy from 2000 to 2024: a bibliometric analysis and integrative overview.Journal of cardiothoracic surgery · 2026Review
- Cell death forms in myocardial ischemia-reperfusion injury and their potential clinical applications.Molecular and cellular biochemistry · 2026Review
- A bibliometric analysis of the literature published on autophagy, ferroptosis, necroptosis, and pyroptosis in cardiovascular disease from 2009 to 2023.Journal of thoracic disease · 2025Article
- Necrosis-like cell death modes in heart failure: the influence of aetiology and the effects of RIP3 inhibition.Basic research in cardiology · 2025Article
- Pharmaceutical Therapies for Necroptosis in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular development and disease · 2023Review
- Essential Amino Acids-Rich Diet Increases Cardiomyocytes Protection in Doxorubicin-Treated Mice.Nutrients · 2023Article
- The MEF2A transcription factor interactome in cardiomyocytes.Cell death & disease · 2023Article
- Serum Dynamin-Related Protein 1 Concentrations Discriminate Phenotypes and Predict Prognosis of Heart Failure.Reviews in cardiovascular medicine · 2023Article
- Perfluorooctane Sulfonate Induces Dysfunction of Human Umbilical Vein Endothelial Cells via Ferroptosis Pathway.Toxics · 2022Article
- Necroptosis in heart disease: Molecular mechanisms and therapeutic implications.Journal of molecular and cellular cardiology · 2022Review
- Interplay of Oxidative Stress and Necrosis-like Cell Death in Cardiac Ischemia/Reperfusion Injury: A Focus on Necroptosis.Biomedicines · 2022Review
- Research on natural products from traditional Chinese medicine in the treatment of myocardial ischemia-reperfusion injury.American journal of translational research · 2022Review
- Therapeutic Peptides to Treat Myocardial Ischemia-Reperfusion Injury.Frontiers in cardiovascular medicine · 2022Review
- Preliminary evidence for the presence of multiple forms of cell death in diabetes cardiomyopathy.Acta pharmaceutica Sinica. B · 2022Review
- TEAD1 protects against necroptosis in postmitotic cardiomyocytes through regulation of nuclear DNA-encoded mitochondrial genes.Cell death and differentiation · 2021Article
- Targeting necroptosis as therapeutic potential in chronic myocardial infarction.Journal of biomedical science · 2021Review
- Klotho attenuates angiotensin II‑induced cardiotoxicity through suppression of necroptosis and oxidative stress.Molecular medicine reports · 2021Article
- RIPK3 Induces Cardiomyocyte Necroptosis via Inhibition of AMPK-Parkin-Mitophagy in Cardiac Remodelling after Myocardial Infarction.Oxidative medicine and cellular longevity · 2021Article
- Ferroptosis Is a Potential Novel Diagnostic and Therapeutic Target for Patients With Cardiomyopathy.Frontiers in cell and developmental biology · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
As cardiomyocytes have a limited capability for proliferation, renewal, and repair, the loss of heart cells followed by replacement with fibrous tissue is considered to result in the development of ventricular dysfunction and progression to heart failure (HF). The loss of cardiac myocytes in HF has been traditionally believed to occur mainly due to programmed apoptosis or unregulated necrosis. While extensive research work is being carried out to define the exact significance and contribution of both these cell death modalities in the development of HF, recent knowledge has indicated the existence and importance of a different form of cell death called necroptosis in the failing heart. This new cell damaging process, resembling some of the morphological features of passive necrosis as well as maladaptive autophagy, is a programmed process and is orchestrated by a complex set of proteins involving receptor-interacting protein kinase 1 and 3 (RIP1, RIP3) and mixed lineage kinase domain-like protein (MLKL). Activation of the RIP1-RIP3-MLKL signaling pathway leads to disruption of cation homeostasis, plasma membrane rupture, and finally cell death. It seems likely that inhibition of any site in this pathway may prove as an effective pharmacological intervention for preventing the necroptotic cell death in the failing heart. This review is intended to describe general aspects of the signaling pathway associated with necroptosis, to describe its relationship with cardiac dysfunction in some models of cardiac injury and discuss its potential relevance in various types of HF with respect to the underlying pathologic mechanisms.
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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.