Evidence map›Paper›PMID 42030645›Full record

ArticleRedox biology2026

Endothelial MerTK impairment promotes cardiac dysfunction in the condition of high fat diet.

Hongye Huang, Shijie Liu, Jingke Yao, Xiaoyuan Bai, Zhicheng Jin, Bingzhong Xue, Hang Shi, Zufeng Ding

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026
    Review
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

8 authors.

Hongye HuangDepartment of Biology, Georgia State University, Atlanta, GA, 30303, USA.
Shijie LiuDepartment of Biology, Georgia State University, Atlanta, GA, 30303, USA.
Jingke YaoDepartment of Biology, Georgia State University, Atlanta, GA, 30303, USA.
Xiaoyuan BaiDepartment of Biology, Georgia State University, Atlanta, GA, 30303, USA.
Zhicheng JinDepartment of Chemistry, Georgia State University, Atlanta, GA, 30303, USA.
Bingzhong XueDepartment of Biology, Georgia State University, Atlanta, GA, 30303, USA.
Hang ShiDepartment of Biology, Georgia State University, Atlanta, GA, 30303, USA.
Zufeng DingDepartment of Biology, Georgia State University, Atlanta, GA, 30303, USA. Electronic address: zding7@gsu.edu.

Funding

Impact of hemodynamics on efferocytosis in endothelial cellsR01HL162958 · NHLBI · UNIV OF ARKANSAS FOR MED SCIS · PI Zufeng Ding · 2022 to 2026
$1.7M
NHLBI NIH HHS R01 HL162958
6 · The paper itself

Abstract

rationaleCardiac fibrosis formation leads to cardiac dysfunction that is mainly caused by a high fat diet accompanied by an increased accumulation of apoptotic cells. MER proto-oncogene tyrosine kinase (MerTK) is a major receptor for efferocytosis, a process for the efficient clearance of apoptotic cells. This study was designed to investigate the novel role of endothelial MerTK in regulating cardiac dysfunction in the condition of high fat diet.

methodsMerTK deficiency in endothelial cells (MerTK

resultsThe proteomics data showed that mitochondrial dysfunction, increased apoptosis and necrosis, defective phagosome formation, and impaired engulfment of cells represent the main signaling pathways involved in endothelial MerTK-mediated cardiac dysfunction. The immunostaining data indicates that endothelial MerTK deficiency promotes NADPH oxidases activation, cardiac fibrosis formation, phenotypic switching in smooth muscle cells (SMCs) and pro-inflammation response, while inhibiting expression of Apolipoprotein E (ApoE), all are key drivers to accelerate cardiac dysfunction. The scRNA-seq analysis in mouse hearts highlights the importance of endothelial functions in cardiac hypertrophy. The snRNA-seq analysis reveals endothelial MerTK dynamics in cardiac dysfunction based on specimens from human patients with dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM).

conclusionsThese findings provide compelling evidence that endothelial MerTK impairment is a novel mechanism in promoting cardiac dysfunction.

Indexed as

c-Mer Tyrosine KinaseDiet, High-FatEndothelial CellsAnimalsApoptosisDisease Models, AnimalEfferocytosisFibrosisHumansMaleMiceMice, KnockoutProteomicsProto-Oncogene Masc-Mer Tyrosine KinaseMAS1 protein, humanMERTK protein, humanMertk protein, mouseProto-Oncogene MasBig data analyticsCardiac dysfunctionEndothelial cellsMerTKscRNA-seq

Identifiers

PMID42030645
PMCPMC13125900

What OpenQuestion holds

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LicenceCC BY
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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.