ArticleAging2019
Targeting CARD6 attenuates spinal cord injury (SCI) in mice through inhibiting apoptosis, inflammation and oxidative stress associated ROS production.
Article in Aging, 2019. 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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Who cites it
20 citing papers in PubMed, 37 citations in OpenAlex.
- Construction of a Computationally Inferred Single-Cell miRNA Activity Atlas and Analysis of Regulatory Networks in Spinal Cord Injury.Journal of molecular neuroscience : MN · 2026Article
- Remimazolam attenuated lipopolysaccharide-induced behavioral deficits and neuronal injury via activation of the Nrf2 pathway.Scientific reports · 2025Article
- The Impact of Nuclear Factor Kappa B on the Response of Microglia in Spinal Cord Injuries.Cureus · 2025Review
- Cordyceps Sinensis Reduces Inflammation and Protects BEAS-2B Cells From LPS-Induced THP-1 Cell Injury.Journal of inflammation research · 2025Article
- The emerging role of cuproptosis in spinal cord injury.Frontiers in immunology · 2025Review
- Crosstalk Between Cell Death and Spinal Cord Injury: Neurology and Therapy.Molecular neurobiology · 2024Review
- The Circadian Clock Gene Bmal1 Regulates Microglial Pyroptosis After Spinal Cord Injury via NF-κB/MMP9.CNS neuroscience & therapeutics · 2024Article
- Bexarotene improves motor function after spinal cord injury in mice.Neural regeneration research · 2023Article
- Molecular Mechanisms for Changing Brain Connectivity in Mice and Humans.International journal of molecular sciences · 2023Article
- Different Ways to Die: Cell Death Pathways and Their Association With Spinal Cord Injury.Neurospine · 2023Article
- Advances in molecular therapies for targeting pathophysiology in spinal cord injury.Expert opinion on therapeutic targets · 2023Review
- The role of apoptosis in spinal cord injury: a bibliometric analysis from 1994 to 2023.Frontiers in cellular neuroscience · 2023Article
- The PI3K/AKT signalling pathway in inflammation, cell death and glial scar formation after traumatic spinal cord injury: Mechanisms and therapeutic opportunities.Cell proliferation · 2022Review
- Transcriptome-wide N6-methyladenine methylation in granulosa cells of women with decreased ovarian reserve.BMC genomics · 2022Article
- MicroRNA-218 aggravates HExperimental and therapeutic medicine · 2021Article
- Programmed cell death in spinal cord injury pathogenesis and therapy.Cell proliferation · 2021Review
- SARM1 promotes neuroinflammation and inhibits neural regeneration after spinal cord injury through NF-κB signaling.Theranostics · 2021Article
- Hematogenous Macrophages: A New Therapeutic Target for Spinal Cord Injury.Frontiers in cell and developmental biology · 2021Review
- Ormosanine improves neuronal functions in spinal cord-injured rats by blocking peroxynitrite/calpain activity.Translational neuroscience · 2020Article
- Systemic Administration of Fibroblast Growth Factor 21 Improves the Recovery of Spinal Cord Injury (SCI) in Rats and Attenuates SCI-Induced Autophagy.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) causes long-term and severe disability, influencing the quality of life and triggering serious socioeconomic consequences. Lack of effective pharmacotherapies for SCI is largely attributable to an incomplete understanding of its pathogenesis. Caspase recruitment domain family member 6 (CARD6) was initially suggested to be a protein playing significant role in NF-κB activation. However, the effects of CARD6 on SCI progression remain unknown. In this study, the wild type (CARD6+/+), CARD6 knockout (CARD6-/-) and CARD6 transgenic (TG) mice were subjected to a SCI model in vivo, and in vitro experiments were conducted by treating microglia cells with lipopolysaccharide (LPS). Here, we identified CARD6 as a suppressor of SCI in mice. CARD6 knockout significantly accelerated functional deficits, neuron death and glia activation, whereas CARD6 overexpression resulted in the opposite effects. Both in vivo and in vitro SCI models suggested that CARD6 knockout markedly promoted apoptosis by increasing Cyto-c release to cytosol from mitochondria and activating Caspase-3 signaling. In addition, CARD6 knockout mice exhibited stronger inflammatory response after SCI, as evidenced by the significantly elevated expression of pro-inflammatory cytokines TNF-α, IL-1β and IL-6, which was largely through enhancing the activation of NF-κB signaling.
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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.