ReviewCellular and molecular life sciences : CMLS2010
Going up in flames: necrotic cell injury and inflammatory diseases.
Review in Cellular and molecular life sciences : CMLS, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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
51 citing papers in PubMed, 99 citations in OpenAlex.
- Electric Cell-Substrate Impedance Sensing as a Tool to Characterize Wound Healing Dynamics.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Regulated Cell Death of Retinal Ganglion Cells in Glaucoma: Molecular Insights and Therapeutic Potentials.Cellular and molecular neurobiology · 2023Review
- Various Forms of Programmed Cell Death Are Concurrently Activated in the Population of Retinal Ganglion Cells after Ischemia and Reperfusion.International journal of molecular sciences · 2023Article
- The Possible Role of Naringenin in the Prevention of Alcohol-Induced Neurochemical and Neurobehavioral Deficits.Neurochemical research · 2023Article
- How do necrotic cells expose phosphatidylserine to attract their predators-What's unique and what's in common with apoptotic cells.Frontiers in cell and developmental biology · 2023Review
- Pterostilbene Ameliorates Fumonisin B1-Induced Cytotoxic Effect by Interfering in the Activation of JAK/STAT Pathway.Antioxidants (Basel, Switzerland) · 2022Article
- GSK872 and necrostatin-1 protect retinal ganglion cells against necroptosis through inhibition of RIP1/RIP3/MLKL pathway in glutamate-induced retinal excitotoxic model of glaucoma.Journal of neuroinflammation · 2022Article
- Multiple types of programmed necrosis such as necroptosis, pyroptosis, oxytosis/ferroptosis, and parthanatos contribute simultaneously to retinal damage after ischemia-reperfusion.Scientific reports · 2022Article
- Circadian Volume Changes in Hippocampal Glia Studied by Label-Free Interferometric Imaging.Cells · 2022Article
- Tumor Necrosis Factor-α Mediates Lung Injury in the Early Phase of Endotoxemia.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Mixed lineage kinase domain-like pseudokinase-mediated necroptosis aggravates periodontitis progression.Journal of molecular medicine (Berlin, Germany) · 2022Article
- Programmed Cell Death Tunes Tumor Immunity.Frontiers in immunology · 2022Review
- Simultaneous Inhibition of Three Major Cytokines and Its Therapeutic Effects: A Peptide-Based Novel Therapy against Endotoxemia in Mice.Journal of personalized medicine · 2021Article
- Calcium ions trigger the exposure of phosphatidylserine on the surface of necrotic cells.PLoS genetics · 2021Article
- Peptide-Based TNF-α-Binding Decoy Therapy Mitigates Lipopolysaccharide-Induced Liver Injury in Mice.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Caspase-8 Regulates Endoplasmic Reticulum Stress-Induced Necroptosis Independent of the Apoptosis Pathway in Auditory Cells.International journal of molecular sciences · 2019Article
- Cell Death Pathways: a Novel Therapeutic Approach for Neuroscientists.Molecular neurobiology · 2018Review
- RIPK1-RIPK3-MLKL-Associated Necroptosis DrivesFrontiers in immunology · 2018Article
- Necroptosis in neurodegenerative diseases: a potential therapeutic target.Cell death & disease · 2017Review
- Necrotic Cells Actively Attract Phagocytes through the Collaborative Action of Two Distinct PS-Exposure Mechanisms.PLoS genetics · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Recent evidence indicates that cell death can be induced through multiple mechanisms. Strikingly, the same death signal can often induce apoptotic as well as non-apoptotic cell death. For instance, inhibition of caspases often converts an apoptotic stimulus to one that causes necrosis. Because a dedicated molecular circuitry distinct from that controlling apoptosis is required for necrotic cell injury, terms such as "programmed necrosis" or "necroptosis" have been used to distinguish stimulus-dependent necrosis from those induced by non-specific traumas (e.g., heat shock) or secondary necrosis induced as a consequence of apoptosis. In several experimental models, programmed necrosis/necroptosis has been shown to be a crucial control point for pathogen- or injury-induced inflammation. In this review, we will discuss the molecular mechanisms that regulate programmed necrosis/necroptosis and its biological significance in pathogen infections, drug-induced cell injury, and trauma-induced tissue damage.
Indexed as
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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.