ArticleJournal of neuroinflammation2018
Myeloid-specific TAK1 deletion results in reduced brain monocyte infiltration and improved outcomes after stroke.
Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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
7 citing papers in PubMed, 9 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
- PARVB deficiency alleviates cisplatin-induced tubular injury by inhibiting TAK1 signaling.Cellular and molecular life sciences : CMLS · 2024Article
- Serpine1 Regulates Peripheral Neutrophil Recruitment and Acts as Potential Target in Ischemic Stroke.Journal of inflammation research · 2022Article
- Microglial-specific depletion of TAK1 is neuroprotective in the acute phase after ischemic stroke.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Age-dependent involvement of gut mast cells and histamine in post-stroke inflammation.Journal of neuroinflammation · 2020Article
- Microglial IRF5-IRF4 regulatory axis regulates neuroinflammation after cerebral ischemia and impacts stroke outcomes.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Monocyte Transmodulation: The Next Novel Therapeutic Approach in Overcoming Ischemic Stroke?Frontiers in neurology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundActivation of transforming growth factor-β-activated kinase 1 (TAK1) occurs after stroke and leads to an exacerbation of brain injury. TAK1 is involved in innate and adaptive immune responses, but it has divergent inflammatory effects that are dependent on the cell type in which it is activated. There is a robust infiltration of myeloid cells after stroke; however, the contribution of myeloid TAK1 to cerebral ischemia is currently unknown. We hypothesized that myeloid-specific deletion of TAK1 would protect against ischemic brain injury.
methodsMyeloid TAK1
resultsInfarcts were significantly smaller in TAK1
conclusionOur results showed that deletion of myeloid TAK1 resulted in smaller infarcts and improved functional outcomes at the peak of inflammation (day 3) and a reduction in brain-infiltrating immune cells that were primarily monocytes. Myeloid TAK1 deletion was also protective at 7 days post MCAo, reflecting a detrimental role of myeloid TAK1 in the progression of ischemic injury.
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.