Evidence map›Paper›PMID 24808360›Full record

Trial reportJournal of immunology (Baltimore, Md. : 1950)2014

CD36-mediated hematoma absorption following intracerebral hemorrhage: negative regulation by TLR4 signaling.

Huang Fang, Jing Chen, Sen Lin, PengFei Wang, YanChun Wang, XiaoYi Xiong, QingWu Yang

Open access · bronzeAbstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.

  1. Pooled it
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  4. Toll like receptor 4 (TLR4) in neuroinflammation: From acute hemorrhagic stroke to chronic neurodegeneration.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
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25 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Huang FangDepartment of Neurology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China;
Jing ChenDepartment of Neurology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China;
Sen LinDepartment of Development and Regeneration Key Laboratory of Sichuan Province, Chengdu Medical College, Chengdu 610083, China; and Department of Histoembryology and Neurobiology, Chengdu Medical College, Chengdu 610083, China.
PengFei WangDepartment of Neurology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China;
YanChun WangDepartment of Neurology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China;
XiaoYi XiongDepartment of Neurology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China;
QingWu YangDepartment of Neurology, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, China; yangqwmlys@hotmail.com.
Army Medical University · CNXinqiao Hospital · CNChengdu Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Promoting hematoma absorption is a novel therapeutic strategy for intracerebral hemorrhage (ICH); however, the mechanism of hematoma absorption is unclear. The present study explored the function and potential mechanism of CD36 in hematoma absorption using in vitro and in vivo ICH models. Hematoma absorption in CD36-deficient ICH patients was examined. Compared with patients with normal CD36 expression, CD36-deficient ICH patients had slower hematoma adsorption and aggravated neurologic deficits. CD36 expression in perihematomal tissues in wild-type mice following ICH was increased, whereas the hematoma absorption in CD36(-/-) mice was decreased. CD36(-/-) mice also showed aggravated neurologic deficits and increased TNF-α and IL-1β expression levels. The phagocytic capacity of CD36(-/-) microglia for RBCs was also decreased. Additionally, the CD36 expression in the perihematoma area after ICH in TLR4(-/-) and MyD88(-/-) mice was significantly increased, and hematoma absorption was significantly promoted, which was significantly inhibited by an anti-CD36 Ab. In vitro, TNF-α and IL-1β significantly inhibited the microglia expression of CD36 and reduced the microglia phagocytosis of RBCs. Finally, the TLR4 inhibitor TAK-242 upregulated CD36 expression in microglia, promoted hematoma absorption, increased catalase expression, and decreased the H2O2 content. These results suggested that CD36 mediated hematoma absorption after ICH, and TLR4 signaling inhibited CD36 expression to slow hematoma absorption. TLR4 inhibition could promote hematoma absorption and significantly improve neurologic deficits following ICH.

Indexed as

AdultAgedAnimalsBlood Platelet DisordersBrain Hemorrhage, TraumaticCatalaseCD36 AntigensFemaleGenetic Diseases, InbornHematoma, Epidural, CranialHumansHydrogen PeroxideMaleMice, KnockoutMicrogliaMiddle AgedCatalaseCD36 AntigensHydrogen PeroxideMyd88 protein, mouseMyeloid Differentiation Factor 88Nerve Tissue ProteinsTLR4 protein, humanTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID24808360
PMCPMC4049082
OpenAlexW2165553751

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.