ReviewJournal of cardiovascular development and disease2023
Pharmaceutical Therapies for Necroptosis in Myocardial Ischemia-Reperfusion Injury.
Review in Journal of cardiovascular development and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- Therapeutic potential of astrocyte transdifferentiated neurons.Neural regeneration research · 2026Article
- MLKL Deficiency Stabilizes RIP3 and Aggravates Myocardial Injury by Promoting Apoptosis and Pyroptosis.Current issues in molecular biology · 2026Article
- Angelica sinensis polysaccharide nanoparticles can improve myocardial ischemia-reperfusion injury by inhibiting ferritinophagy via the ATF6/NCOA4 pathway.Journal of translational medicine · 2026Article
- Oxidative Stress andInternational journal of molecular sciences · 2026Review
- Mitochondrial homeostasis meets novel programmed cell death: crosstalk mechanisms underlying cardiovascular diseases progression.Cell communication and signaling : CCS · 2026Review
- Delaying cardiac aging: potential mechanisms centered on PANoptosis and targeted intervention strategies.Frontiers in cardiovascular medicine · 2026Review
- Systematic Pharmacology Combined With Experimental Validation Reveals the Apoptosis-Related Mechanism of Simiao Yong'an (SMYA) Decoction Against Myocardial Ischemia-Reperfusion Injury.Cardiovascular therapeutics · 2026Article
- Activation of the cGAS-STING Pathway by NETs Promotes Inflammatory Injury in Myocardial Ischemia-Reperfusion.Journal of inflammation research · 2026Article
- Artificial intelligence-enabled discovery of a RIPK3 inhibitor with neuroprotective effects in an acute glaucoma mouse model.Chinese medical journal · 2025Article
- β-sitosterol ameliorates myocardial infarction injury via modulating the NF-κB and necroptosis signaling pathways.Frontiers in pharmacology · 2025Article
- Regulated cell death and DAMPs as biomarkers and therapeutic targets in normothermic perfusion of transplant organs. Part 1: their emergence from injuries to the donor organ.Frontiers in transplantation · 2025Review
- The role of IFI16 in regulating PANoptosis and implication in heart diseases.Cell death discovery · 2024Review
- CircBAZ1B stimulates myocardial ischemia/reperfusion injury (MI/RI) by modulating miR-1252-5p/ATF3-mediated ferroptosis.Archives of medical science : AMS · 2024Article
- Downregulation of RIP3 ameliorates the left ventricular mechanics and function after myocardial infarctionOpen life sciences · 2024Article
- Is Intrinsic Cardioprotection a Laboratory Phenomenon or a Clinically Relevant Tool to Salvage the Failing Heart?International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular disease morbidity/mortality are increasing due to an aging population and the rising prevalence of diabetes and obesity. Therefore, innovative cardioprotective measures are required to reduce cardiovascular disease morbidity/mortality. The role of necroptosis in myocardial ischemia-reperfusion injury (MI-RI) is beyond doubt, but the molecular mechanisms of necroptosis remain incompletely elucidated. Growing evidence suggests that MI-RI frequently results from the superposition of multiple pathways, with autophagy, ferroptosis, and CypD-mediated mitochondrial damage, and necroptosis all contributing to MI-RI. Receptor-interacting protein kinases (RIPK1 and RIPK3) as well as mixed lineage kinase domain-like pseudokinase (MLKL) activation is accompanied by the activation of other signaling pathways, such as Ca
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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.