ArticleCell reports2016
TMEM16F Regulates Spinal Microglial Function in Neuropathic Pain States.
Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 62 citations in OpenAlex.
- Glial cells in neuropathic pain.Physiological reviews · 2026Review
- Lipid flip-flop in biological membranes: through the lens of TMEM16F.Physiological reviews · 2026Review
- Calcium dependent activation of the TMEM16F scramblase and ion channel.Nature structural & molecular biology · 2026Article
- Targeting microglia microtubules: cytoskeletal remodeling as a druggable hub in neuroinflammation and neurodegeneration.Frontiers in neuroscience · 2026Review
- The chloride intracellular channel 1 (CLIC1) is essential for microglial morphodynamics and neuroinflammation.Science advances · 2025Article
- Article
- Spi1 aggravates neuropathic pain by modulating Clec7a-mediated neuroinflammation and microglial phagocytosis.The journal of headache and pain · 2025Article
- Sex-Related Differences in Chronic Pain: A Narrative Review by a Multidisciplinary Task Force.Medicina (Kaunas, Lithuania) · 2025Review
- Targeting C1q prevents microglia-mediated synaptic removal in neuropathic pain.Nature communications · 2025Article
- How microglia contribute to the induction and maintenance of neuropathic pain.Nature reviews. Neuroscience · 2025Review
- Spinal Cord Microglia in the Development of Touch.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- TMEM16F exacerbates tau pathology and mediates phosphatidylserine exposure in phospho-tau-burdened neurons.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Immune drivers of physiological and pathological pain.The Journal of experimental medicine · 2024Article
- Microglial Refinement of A-Fiber Projections in the Postnatal Spinal Cord Dorsal Horn Is Required for Normal Maturation of Dynamic Touch.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Review
- PLSCR1 promotes apoptosis and clearance of retinal ganglion cells in glaucoma pathogenesis.Genes & diseases · 2023Article
- TMEM16F may be a new therapeutic target for Alzheimer's disease.Neural regeneration research · 2023Article
- Activation of β2-Adrenergic Receptors in Microglia Alleviates Neuropathic Hypersensitivity in Mice.Cells · 2023Article
- Generation of human TMEM16F-specific affibodies using purified TMEM16F.Frontiers in molecular biosciences · 2023Article
- Basic mechanisms of peripheral nerve injury and treatment via electrical stimulation.Neural regeneration research · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuropathic pain is a widespread chronic pain state that results from injury to the nervous system. Spinal microglia play a causative role in the pathogenesis of neuropathic pain through secretion of growth factors and cytokines. Here, we investigated the contribution of TMEM16F, a protein that functions as a Ca(2+)-dependent ion channel and a phospholipid scramblase, to microglial activity during neuropathic pain. We demonstrate that mice with a conditional ablation of TMEM16F in microglia do not develop mechanical hypersensitivity upon nerve injury. In the absence of TMEM16F, microglia display deficits in process motility and phagocytosis. Moreover, loss of GABA immunoreactivity upon injury is spared in TMEM16F conditional knockout mice. Collectively, these data indicate that TMEM16F is an essential component of the microglial response to injury and suggest the importance of microglial phagocytosis in the pathogenesis of neuropathic pain.
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.