Evidence map›Paper›PMID 39179950›Full record

ArticleJournal of thrombosis and thrombolysis2025

Ghrelin may protect against vascular endothelial injury in Acute traumatic coagulopathy by mediating the RhoA/ROCK/MLC2 pathway.

Chengjian He, Xiaojing Song, Zigui Zhu, Yan Xiao, Jiacheng Chen, Hongyi Yao, Rongjun Xie

Erratum issuedAbstract read
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In one paragraph

Article in Journal of thrombosis and thrombolysis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Chengjian He *Affiliated Nanhua Hospital, University of South China, No. 336, Dongfeng South Road Zhuhui District, Hengyang City, Hunan Province, China.
Xiaojing Song *Affiliated Nanhua Hospital, University of South China, No. 336, Dongfeng South Road Zhuhui District, Hengyang City, Hunan Province, China.
Zigui ZhuAffiliated Nanhua Hospital, University of South China, No. 336, Dongfeng South Road Zhuhui District, Hengyang City, Hunan Province, China.
Yan XiaoAffiliated Nanhua Hospital, University of South China, No. 336, Dongfeng South Road Zhuhui District, Hengyang City, Hunan Province, China.
Jiacheng ChenAffiliated Nanhua Hospital, University of South China, No. 336, Dongfeng South Road Zhuhui District, Hengyang City, Hunan Province, China.
Hongyi YaoAffiliated Nanhua Hospital, University of South China, No. 336, Dongfeng South Road Zhuhui District, Hengyang City, Hunan Province, China.
Rongjun XieAffiliated Nanhua Hospital, University of South China, No. 336, Dongfeng South Road Zhuhui District, Hengyang City, Hunan Province, China. xierongjuntx@126.com.ORCID http://orcid.org/0009-0007-5131-4287

Funding

Innovative Research Group Project of the National Natural Science Foundation of China 81873649Scientific Research Project of Hunan Provincial Health Commission in 2020 20201951
6 · The paper itself

Abstract

Ghrelin exerts widespread effects in several diseases, but its role and mechanism in Acute Traumatic Coagulopathy (ATC) are largely unknown. The effect of ghrelin on cell proliferation was examined using three assays: 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), Lactate Dehydrogenase (LDH), and flow cytometry. The barrier function of the endothelial cells was evaluated using the Trans-Endothelial Electrical Resistance (TEER) and the endothelial permeability assay. An ATC mouse model was established to evaluate the in vivo effects of ghrelin. The Ras homolog family member A (RhoA) overexpression plasmid or adenovirus was used to examine the molecular mechanism of ghrelin. Ghrelin enhanced Human Umbilical Vein Endothelial Cells (HUVEC) proliferation and endothelial cell barrier function and inhibited HUVEC permeability damage in vitro. Additionally, ghrelin decreased the activated Partial Thromboplastin Time (aPTT) and Prothrombin Time (PT) in mice blood samples in the ATC mouse model. Ghrelin also improved the pathological alterations in postcava. Mechanistically, ghrelin acts through the RhoA/ Rho-associated Coiled-coil Containing Kinases (ROCK)/ Myosin Light Chain 2 (MLC2) pathway. Furthermore, the protective effects of ghrelin, both in vitro and in vivo, were reversed by RhoA overexpression. Our findings demonstrate that ghrelin may reduce vascular endothelial cell damage and endothelial barrier dysfunction by blocking the RhoA pathway, suggesting that ghrelin may serve as a potential therapeutic target for ATC treatment.

Indexed as

Blood Coagulation DisordersCardiac MyosinsEndothelium, VascularGhrelinMyosin Light ChainsrhoA GTP-Binding Proteinrho-Associated KinasesWounds and InjuriesAnimalsCell ProliferationDisease Models, AnimalHumansHuman Umbilical Vein Endothelial CellsMaleMiceSignal TransductionCardiac MyosinsGhrelinmyosin light chain 2Myosin Light ChainsrhoA GTP-Binding ProteinRHOA protein, humanrho-Associated KinasesAcute traumatic coagulopathyEndothelial barrierEndothelial cellsGhrelin

Identifiers

PMID39179950
PMCPMC11762449

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.