ArticleJournal of the American Heart Association2020
CARD3 Promotes Cerebral Ischemia-Reperfusion Injury Via Activation of TAK1.
Article in Journal of the American Heart Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Regulation of G Protein Signaling 14 protects against cerebral ischemic reperfusion injury by inhibiting the TAK1-JNK/p38 signaling pathway.Histology and histopathology · 2026Article
- Gut-brain axis modulation by fecal microbiota transplantation improves dual-organ injury after cerebral ischemia-reperfusion via Caspase-8 dependent inhibition of necroptosis.Metabolic brain disease · 2026Article
- Pathological mechanisms and therapeutic potential of MSC-Exos in ischemic stroke management.Stem cell research & therapy · 2026Review
- Crosstalk between autophagy-dependent ferroptosis and PANoptosis in myocardial and cerebral ischemia-reperfusion injury: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- The Therapeutic Potential of Garlic-Derived Organic Polysulfides for Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
- E2F1/CDK5/DRP1 axis mediates microglial mitochondrial division and autophagy in the pathogenesis of cerebral ischemia-reperfusion injury.Clinical and translational medicine · 2025Article
- TNFSF9 Silence Impedes Cerebral Ischemia-Reperfusion Injury via Modulating SLC3A2 Expression in Brain Microvascular Endothelial Cells.Journal of molecular neuroscience : MN · 2025Article
- Exosomes: an innovative therapeutic target for cerebral ischemia-reperfusion injury.Frontiers in pharmacology · 2025Review
- PANoptosis: a new insight into the mechanism of ischaemia-reperfusion injury.Burns & trauma · 2025Review
- Nek6 regulates autophagy through the mTOR signaling pathway to alleviate cerebral ischemia-reperfusion injury.Molecular brain · 2024Article
- RIPK2 Is Crucial for the Microglial Inflammatory Response to Bacterial Muramyl Dipeptide but Not to Lipopolysaccharide.International journal of molecular sciences · 2024Article
- RIPK2 is crucial for the microglial inflammatory response to bacterial muramyl dipeptide but not to lipopolysaccharide.bioRxiv : the preprint server for biology · 2024Article
- The Protective Role of Transcript-Induced in Spermiogenesis 40 in Cerebral Ischemia-Reperfusion Injury.Neurochemical research · 2024Article
- Unraveling the molecular complexity: Wtap/Ythdf1 and Lcn2 in novel traumatic brain injury secondary injury mechanisms.Cell biology and toxicology · 2024Article
- Current progression in application of extracellular vesicles in central nervous system diseases.European journal of medical research · 2024Review
- Insight into interplay between PANoptosis and autophagy: novel therapeutics in ischemic stroke.Frontiers in molecular neuroscience · 2024Review
- Neurotoxic β-amyloid oligomers cause mitochondrial dysfunction-the trigger for PANoptosis in neurons.Frontiers in aging neuroscience · 2024Review
- Mitochondrial dysfunctions induce PANoptosis and ferroptosis in cerebral ischemia/reperfusion injury: from pathology to therapeutic potential.Frontiers in cellular neuroscience · 2023Review
- Do pyroptosis, apoptosis, and necroptosis (PANoptosis) exist in cerebral ischemia? Evidence from cell and rodent studies.Neural regeneration research · 2022Article
- Activated Drp1 regulates p62-mediated autophagic flux and aggravates inflammation in cerebral ischemia-reperfusion via the ROS-RIP1/RIP3-exosome axis.Military Medical Research · 2022Article
Corrections and comments
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Authors and funding
19 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Although multiple signaling cascades and molecules contributing to the pathophysiological process have been studied, the treatments for stroke against present targets have not acquired significant clinical progress. Although CARD3 (caspase activation and recruitment domain 3) protein is an important factor involved in regulating immunity, inflammation, lipid metabolism, and apoptosis, its role in cerebral stroke is currently unknown. Methods and Results Using a mouse model of ischemia-reperfusion (I-R) injury based on transient blockage of the middle cerebral artery, we have found that CARD3 expression is upregulated in a time-dependent manner during I-R injury. Further animal study revealed that, relative to control mice, CARD3-knockout mice exhibited decreased inflammatory response and neuronal apoptosis, with reduced infarct volume and lower neuropathological scores. In contrast, neuron-specific CARD3-overexpressing transgenic (CARD3-TG) mice exhibited increased I-R induced injury compared with controls. Mechanistically, we also found that the activation of TAK1 (transforming growth factor-β-activated kinase 1) was enhanced in CARD3-TG mice. Furthermore, the increased inflammation and apoptosis seen in injured CARD3-TG brains were reversed by intravenous administration of the TAK1 inhibitor 5Z-7-oxozeaenol. Conclusions These results indicate that CARD3 promotes I-R injury via activation of TAK1, which not only reveals a novel regulatory axis of I-R induced brain injury but also provides a new potential therapeutic approach for I-R 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.