ArticleNature neuroscience2020
Reversal of prolonged obesity-associated cerebrovascular dysfunction by inhibiting microglial Tak1.
Article in Nature neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 41 citations in OpenAlex.
- Lipid metabolism, microglia, and stroke.Neural regeneration research · 2026Article
- Understanding TAK1 deficiency in microglia: Dual mechanisms for photoreceptor protection in a mouse model of retinitis pigmentosa.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Association between increased BMI and cognitive function in first-episode drug-naïve male schizophrenia.Frontiers in psychiatry · 2024Article
- TAK1 in Vascular Signaling: "Friend or Foe"?Journal of inflammation research · 2024Review
- Noteworthy perspectives on microglia in neuropsychiatric disorders.Journal of neuroinflammation · 2023Review
- Prenatal programing of motivated behaviors: can innate immunity prime behavior?Neural regeneration research · 2023Review
- Takinib inhibits microglial M1 polarization and oxidative damage after subarachnoid hemorrhage by targeting TAK1-dependent NLRP3 inflammasome signaling pathway.Frontiers in immunology · 2023Article
- The diverse roles of macrophages in metabolic inflammation and its resolution.Frontiers in cell and developmental biology · 2023Review
- Microglial phagocytosis and regulatory mechanisms after stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Article
- TRIM45 causes neuronal damage by aggravating microglia-mediated neuroinflammation upon cerebral ischemia and reperfusion injury.Experimental & molecular medicine · 2022Article
- Maternal high-fat diet in mice induces cerebrovascular, microglial and long-term behavioural alterations in offspring.Communications biology · 2022Article
- Hypothalamic long noncoding RNA AK044061 is involved in the development of dietary obesity in mice.International journal of obesity (2005) · 2021Article
- Stimulation of hypothalamic oxytocin neurons suppresses colorectal cancer progression in mice.eLife · 2021Article
- Microglial lnc-U90926 facilitates neutrophil infiltration in ischemic stroke via MDH2/CXCL2 axis.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- TAK1 mediates neuronal pyroptosis in early brain injury after subarachnoid hemorrhage.Journal of neuroinflammation · 2021Article
- Regeneration of Damaged Tendon-Bone Junctions (Entheses)-TAK1 as a Potential Node Factor.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prolonged obesity is associated with cerebrovascular dysfunction; however, the underlying mechanisms remain largely unclear. In the present study, using a prolonged obesity mouse model that suffers from basilar artery (BA) abnormalities, we find that microglial transforming growth factor β-activated kinase 1 (Tak1) is over-activated in the brainstem. Both pharmacological inhibition primarily in the brainstem and genetic microglia-selective deletion of Tak1 ameliorated BA vascular dysfunction. Conversely, microglia-specific activation of Tak1 in the brainstem was sufficient to cause an impairment in BA function in chow-fed mice. Mechanistically, Tak1 activation leads to increased interleukin-18 (IL-18) production, whereas blockade of IL-18 receptor in the brain helped protect against cerebrovascular dysfunction despite prolonged obesity. Microglia-selective deletion of Tak1 also protects against ischemic stroke in prolonged obesity. Taken together, these findings provide evidence that microglial Tak1 in the brain, and particularly the brainstem, contributes to the pathogenesis of obesity-associated cerebrovascular dysfunction.
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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.