Evidence map›Paper›PMID 41952190›Full record

ArticleBMC medicine2026

Apolipoprotein C3 drives adverse cardiac remodeling in ischemic heart failure.

Yufei Han, Yixue Zhao, Zihao Zhou, Changyun Liu, Jinxuan Chen, Guolin Miao, Ling Zhang, Yuhui Wang, Jianping Li, Wei Huang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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

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

11 authors.

Yufei Han *Institute of Cardiovascular Sciences, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Yixue Zhao *Department of Cardiology, Peking University First Hospital, No.8 Xishiku Street, Xicheng District, Beijing, China.
Zihao ZhouInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Changyun LiuInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Jinxuan ChenInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Guolin MiaoInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Ling ZhangInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Yuhui WangInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Jianping LiState Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing, China. lijianping03455@pkufh.com.
Wei HuangInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China. huangwei@bjmu.edu.cn.
Xunde XianInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China. xianxunde@bjmu.edu.cn.

Funding

Beijing Natural Science Foundation 7242084National Key Research and Development Program of China 2021YFC2500600/2021YFC2500601National Natural Science Foundation of China 81770448 and 82370454National Natural Science Foundation of China 82070458 and 82370442National Natural Science Foundation of China 82270479, U25C2004 and HY2021-1
6 · The paper itself

Abstract

backgroundIschemic heart failure (IHF) is one of the leading causes of death in the world. Plasma apolipoprotein C3 (ApoC3) levels are significantly elevated in patients with heart failure and positively associated with the incidence of ischemic heart disease (IHD). However, the causal association between ApoC3 and IHD development is unclear.

methodsApoC3 expression changes were assessed in plasma from IHF patients/healthy donors and cardiac tissue from rodent models. 10-week-old male human ApoC3 transgenic (ApoC3

resultsOverexpression of human ApoC3 in ApoC3

conclusionsApoC3 overexpression could activate cardiac TLR2/NF-κB to trigger the inflammation, oxidation, and apoptosis pathways, finally aggravating IHF in mice. Inactivation of ApoC3 could significantly alleviate IHF in hamsters.

Indexed as

Apolipoprotein C-IIIHeart FailureMyocardial IschemiaVentricular RemodelingAnimalsApoptosisCricetinaeDisease Models, AnimalHumansMaleMiceMice, KnockoutMice, TransgenicNF-kappa BOxidative StressAPOC3 protein, humanApolipoprotein C-IIINF-kappa BApolipoprotein C3ApoptosisInflammationIschemic heart failureOxidation

Identifiers

PMID41952190
PMCPMC13173940

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.