ArticleInflammation2025
TREML2 Modulates Microglial Phagocytosis of Myelin Debris via TLR9 in Chronic Cerebral Ischemia.
Article in Inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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Who cites it
1 citing paper in PubMed.
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Demyelination is a significant pathological feature of chronic cerebral ischemia. Recent evidence suggested that microglia played a protective role in mitigating brain ischemic injury via phagocytosis of myelin debris resulting from demyelination. Triggering receptor expressed on myeloid cells-like 2 (TREML2) is a newly discovered inflammation-associated transmembrane receptor expressed by microglia. To date, whether microglial TREML2 contributes to the phagocytosis of myelin debris in chronic cerebral ischemia has not been fully clarified. In this study, employing a bilateral carotid artery stenosis animal model and a CoCl
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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.