ArticleOncotarget2017
The degradation of mixed lineage kinase domain-like protein promotes neuroprotection after ischemic brain injury.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The trial behind it
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Who cites it
20 citing papers in PubMed, 29 citations in OpenAlex.
- Evaluation of Prognostic Implication of Serum Mixed Lineage Kinase Domain-Like Protein in Acute Primary Supratentorial Intracerebral Hemorrhage: A Multicenter Prospective Cohort Study.Brain and behavior · 2025Article
- Die Hard: Necroptosis and its Impact on Age-Dependent Neuroinflammatory Diseases.Frontiers in cell death · 2024Article
- Insight into interplay between PANoptosis and autophagy: novel therapeutics in ischemic stroke.Frontiers in molecular neuroscience · 2024Review
- Alteration of Serum MLKL Levels and Their Association with Severity and Clinical Outcomes in Human Severe Traumatic Brain Injury: A Prospective Cohort Study.International journal of general medicine · 2024Article
- Necrostatin-1: a promising compound for neurological disorders.Frontiers in cellular neuroscience · 2024Review
- Necrosulfonamide exerts neuroprotective effect by inhibiting necroptosis, neuroinflammation, and α-synuclein oligomerization in a subacute MPTP mouse model of Parkinson's disease.Scientific reports · 2023Article
- From (Tool)Bench to Bedside: The Potential of Necroptosis Inhibitors.Journal of medicinal chemistry · 2023Review
- The brain protection of MLKL inhibitor necrosulfonamide against focal ischemia/reperfusion injury associating with blocking the nucleus and nuclear envelope translocation of MLKL and RIP3K.Frontiers in pharmacology · 2023Article
- Neonatal Arterial Ischaemic Stroke: Advances in Pathologic Neural Death, Diagnosis, Treatment, and Prognosis.Current neuropharmacology · 2022Review
- The regulation of necroptosis and perspectives for the development of new drugs preventing ischemic/reperfusion of cardiac injury.Apoptosis : an international journal on programmed cell death · 2022Review
- Cell-specific activation of RIPK1 and MLKL after intracerebral hemorrhage in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Article
- Insight into Crosstalk between Ferroptosis and Necroptosis: Novel Therapeutics in Ischemic Stroke.Oxidative medicine and cellular longevity · 2021Review
- Emerging immune and cell death mechanisms in stroke: Saponins as therapeutic candidates.Brain, behavior, & immunity - health · 2020Review
- The Role of RIPK1 and RIPK3 in Cardiovascular Disease.International journal of molecular sciences · 2020Review
- Necroptosis in Intestinal Inflammation and Cancer: New Concepts and Therapeutic Perspectives.Biomolecules · 2020Review
- The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia.Oxidative medicine and cellular longevity · 2020Review
- Current translational potential and underlying molecular mechanisms of necroptosis.Cell death & disease · 2019Review
- Necroptosis is one of the modalities of cell death accompanying ischemic brain stroke: from pathogenesis to therapeutic possibilities.Croatian medical journal · 2019Review
- Necrosulfonamide Ameliorates Neurological Impairment in Spinal Cord Injury by Improving Antioxidative Capacity.Frontiers in pharmacology · 2019Article
- Transplantation of neural stem cells in the mouse model of ischemic brain stroke and expression of genes involved in programmed cell death.Croatian medical journal · 2018Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mixed lineage kinase domain-like (MLKL) protein was recently found to play a critical role in necrotic cell death. To explore its role in neurological diseases, we measured MLKL protein expression after ischemia injury in a mouse model. We found that MLKL expression significantly increased 12 h after ischemia/reperfusion (I/R) injury with peak levels at 48 h. Inhibition of MLKL by intraperitoneal administration of NSA significantly reduced infarct volume and improved neurological deficits after 75 min of ischemia and 24 h of reperfusion. Further, we found NSA reduced MLKL levels via the ubiquitination proteasome pathway, but not by inhibiting RNA transcription. Interestingly, NSA administration increased cleaved PARP-1 levels, indicating the protective effects of MLKL inhibition is not related to apoptosis. These findings suggest MLKL is a new therapeutic target for neurological pathologies like stroke. Therefore, promoting degradation of MLKL may be a novel avenue to reduce necrotic cell death after ischemic brain injury.
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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.