ReviewJournal of molecular cell biology2021
The molecular mechanisms of MLKL-dependent and MLKL-independent necrosis.
Review in Journal of molecular cell biology, 2021. 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, 58 citations in OpenAlex.
- Pooled it
- [Role of programmed cell death in platinum resistance in ovarian cancer].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026Review
- Interferon-γ selectively promotes survival of alveolar progenitor cells in a human lung organoid model.The EMBO journal · 2026Article
- SARS-CoV-2-infected cardiomyocytes exhibit upregulated necroptosis, but no evidence of mitochondrial permeability transition.Journal of molecular and cellular cardiology plus · 2026Article
- Non-canonical cell death in neurodegeneration: emerging mechanisms and therapeutic Frontiers.Apoptosis : an international journal on programmed cell death · 2026Review
- Calcium homeostasis imbalance in sepsis: molecular mechanisms and therapeutic perspectives.Frontiers in medicine · 2026Review
- Ferroptosis in Toxicology: Present and Future.International journal of molecular sciences · 2025Review
- Inflammatory adhesion mediates myocardial segmental necroptosis induced by mixed lineage kinase domain-like protein in acute myocardial infarction.Cell communication and signaling : CCS · 2025Article
- Necroptosis and autophagy in cisplatinum-triggered nephrotoxicity: Novel insights regarding their prognostic and diagnostic potential.Toxicology reports · 2024Article
- Regulation of Zfp36 by ISGF3 and MK2 restricts the expression of inflammatory cytokines during necroptosis stimulation.Cell death & disease · 2024Article
- PBI-05204, a supercritical CONeoplasia (New York, N.Y.) · 2024Article
- Necroptosis enhances 'don't eat me' signal and induces macrophage extracellular traps to promote pancreatic cancer liver metastasis.Nature communications · 2024Article
- Research Progress on Micro(nano)plastic-Induced Programmed Cell Death Associated with Disease Risks.Toxics · 2024Review
- Investigation of Lung Cancer Cell Response to Cryoablation and Adjunctive Gemcitabine-Based Cryo-Chemotherapy Using the A549 Cell Line.Biomedicines · 2024Article
- The role of regulated necrosis in diabetes and its complications.Journal of molecular medicine (Berlin, Germany) · 2024Review
- Ferroptosis: a new hunter of hepatocellular carcinoma.Cell death discovery · 2024Review
- Targeting cell death pathways in intestinal ischemia-reperfusion injury: a comprehensive review.Cell death discovery · 2024Review
- Downregulation of Mitochondrial Fusion Protein Expression Affords Protection from Canonical Necroptosis in H9c2 Cardiomyoblasts.International journal of molecular sciences · 2024Article
- Polyunsaturated fatty acids-induced ferroptosis suppresses pancreatic cancer growth.Scientific reports · 2024Article
- Ferroptosis and myocardial ischemia-reperfusion: mechanistic insights and new therapeutic perspectives.Frontiers in pharmacology · 2024Review
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Necrosis, a type of unwanted and passive cell demise, usually occurs under the excessive external stress and is considered to be unregulated. However, under some special conditions such as caspase inhibition, necrosis is regulable in a well-orchestrated way. The term 'regulated necrosis' has been proposed to describe such programed necrosis. Recently, several forms of necrosis, including necroptosis, pyroptosis, ferroptosis, parthanatos, oxytosis, NETosis, and Na+/K+-ATPase-mediated necrosis, have been identified, and some crucial regulators governing regulated necrosis have also been discovered. Mixed lineage kinase domain-like pseudokinase (MLKL), a core regulator in necroptosis, acts as an executioner in response to ligands of death receptor family. Its activation requires the receptor-interacting protein kinases, RIP1 and RIP3. However, MLKL is only involved in necroptosis, i.e. MLKL is dispensable for necrosis. Therefore, this review is aimed at summarizing the molecular mechanisms of MLKL-dependent and MLKL-independent necrosis.
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.