Evidence map›Paper›PMID 42644248›Full record

ArticleCirculation research2026

Hepatic ChREBP Drives Cardiac Remodeling via ApoM Non-transcriptional Repression.

Shuang Zhang, Zhenzhen Zhang, Zihan Ma, Wen Wu, Lu Tang, Yanlu Han, Songning Chen, Tengteng Yan, Ye Chen, Junwu Liu and 9 more

Abstract read
In one paragraph

Article in Circulation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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

19 authors.

Shuang Zhang *School of Food and Biological Engineering, Hefei University of Technology, China (S.Z., L.T., Y.H., S.C., T.Y.).ORCID 0000-0002-8000-4305
Zhenzhen Zhang *Key Laboratory of Bioactive Materials, Ministry of Education (Z.Z., J.L., D.K.), College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Zihan Ma *Frontiers Science Center for Cell Responses (Z.M., B.S.), College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.ORCID 0009-0005-4990-9121
Wen WuDepartment of General Surgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China (W.W.).
Lu TangSchool of Food and Biological Engineering, Hefei University of Technology, China (S.Z., L.T., Y.H., S.C., T.Y.).
Yanlu HanSchool of Food and Biological Engineering, Hefei University of Technology, China (S.Z., L.T., Y.H., S.C., T.Y.).
Songning ChenSchool of Food and Biological Engineering, Hefei University of Technology, China (S.Z., L.T., Y.H., S.C., T.Y.).
Tengteng YanSchool of Food and Biological Engineering, Hefei University of Technology, China (S.Z., L.T., Y.H., S.C., T.Y.).
Ye ChenThe Department of Pathology of the First Affiliated Hospital of Anhui Medical University, Hefei, China (Y.C.).ORCID 0009-0009-4310-5455
Junwu LiuKey Laboratory of Bioactive Materials, Ministry of Education (Z.Z., J.L., D.K.), College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.ORCID 0009-0002-9281-6121
Dongdong JianZhengzhou Key Laboratory of Cardiovascular Aging, Henan Province Key Laboratory for Prevention and Treatment of Coronary Heart Disease, National Health Commission Key Laboratory of Cardiovascular Regenerative Medicine, Central China Fuwai Hospital of Zhengzhou University, Fuwai Central China Cardiovascular Hospital and Central China Branch of National Center for Cardiovascular Diseases, China (D.J.).
Ji'e YangDepartment of Cardiology, the First Affiliated Hospital of USTC, Division of Life Sciences and Medicine (J.Y., L.M., Z.Y., Y.D.), University of Science and Technology of China, Hefei, China.
Likun MaSchool of Food and Biological Engineering, Hefei University of Technology, China (S.Z., L.T., Y.H., S.C., T.Y.).ORCID 0000-0002-9680-1472
Zequn YinSchool of Food and Biological Engineering, Hefei University of Technology, China (S.Z., L.T., Y.H., S.C., T.Y.).
Houzao ChenDepartment of Biochemistry & Molecular Biology, State Key Laboratory of Common Mechanism Research for Major Diseases, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China (H.C.).ORCID 0000-0001-6805-3182
Baofa SunFrontiers Science Center for Cell Responses (Z.M., B.S.), College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.ORCID 0000-0002-8221-1279
Deling KongKey Laboratory of Bioactive Materials, Ministry of Education (Z.Z., J.L., D.K.), College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.ORCID 0000-0002-2961-9267
Junbo GeDepartment of Cardiology, Zhongshan Hospital, Fudan University, Shanghai Institute of Cardiovascular Diseases, China (J.G.).ORCID 0000-0002-9360-7332
Yajun DuanSchool of Food and Biological Engineering, Hefei University of Technology, China (S.Z., L.T., Y.H., S.C., T.Y.).ORCID 0000-0002-3880-9070

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPathological cardiac remodeling is a hallmark of numerous cardiovascular diseases and develops into heart failure. As a systemic disease, effective treatments for cardiac remodeling from a tissue crosstalk perspective are still significantly unmet.

methodsHepatocyte-specific ChREBP (carbohydrate response element binding protein) knockout (KO) or overexpressed mice, global ApoM (apolipoprotein M) KO and adeno-associated virus-mediated hepatic ApoM knockdown or overexpressed mice, cardiomyocyte-specific ChREBP overexpressed mice, as well as S1PR1 (sphingosine-1-phosphate receptor 1) knockdown mice were used in isoproterenol- or transverse aortic constriction-induced cardiac remodeling models. RNA sequencing and liquid chromatography - tandem mass spectrometry (LC-MS/MS) analysis were used to detect changed pathways and the interaction between ChREBP and SURF4 (surfeit 4).

resultsWe found increased ChREBP expression in the liver, but not in the heart, especially in the cytosol of hepatocytes, but not the nucleus, in isoproterenol- or transverse aortic constriction-induced mice. Hepatocyte-specific ChREBP deficiency protected against isoproterenol or transverse aortic constriction-induced cardiac remodeling. Mechanistically, hepatocyte ChREBP deficiency increased ApoM expression in the liver and its secretion, not by transcriptional regulation of ApoM, but by increasing its secretion through the release of SURF4. ApoM overexpression in the liver or ApoM-containing high-density lipoprotein (HDL) injection can both ameliorate cardiac remodeling through the S1P (sphingosine-1-phosphate)/S1PR1 pathway in the heart.

conclusionsThis work identifies the hepatic ChREBP-SURF4-ApoM axis as a critical pathway in cardiac remodeling, and induction of hepatic ApoM secretion constitutes a new promising approach for treating cardiac remodeling and heart failure.

Indexed as

LiverVentricular RemodelingAnimalsHepatocytesMaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacSphingosine-1-Phosphate ReceptorsS1pr1 protein, mouseSphingosine-1-Phosphate Receptorsapolipoproteins Mcardiomegalyheart failuretranscription factorsventricular remodeling

Identifiers

PMID42644248
PMCPMC13608343

What Socratic holds

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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 Socratic graph.