Evidence map›Paper›PMID 41255216›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026

Seipin-Mediated Lipid Droplet Formation in Cardiomyocytes Ameliorates Cardiac Ischemia/Reperfusion Injury.

Changyun Liu, Junxia Zhang, Yusi Chen, Geng Shen, Yufei Han, Zihao Zhou, Jinxuan Chen, Xuya Kang, Huilin Qu, Jiaxin Duanmu and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 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. Article
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

14 authors.

Changyun LiuInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.ORCID https://orcid.org/0000-0002-1393-7578
Junxia ZhangInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Yusi ChenInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Geng ShenDepartment of Cardiology, Beijing Anzhen Hospital, Capital Medical University, Beijing, 100029, China.
Yufei HanInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Zihao ZhouInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Jinxuan ChenInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Xuya KangInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Huilin QuInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Jiaxin DuanmuInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Haibao ShangState Key Laboratory of Membrane Biology, Institute of Molecular Medicine, College of Future Technology, Peking University, Beijing, 100871, China.
Yingjia LiInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.
Wei HuangInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.ORCID https://orcid.org/0009-0005-5164-9744
Yan ZhangInstitute of Cardiovascular Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, 100191, China.ORCID https://orcid.org/0000-0002-8322-467X

Funding

China Postdoctoral Science Foundation 2022M720288China Postdoctoral Science Foundation BX20220023National Key R&D Program of China 2018YFA0800501National Key R&D Program of China 2021YFF0501401National Natural Science Foundation of China 82300286National Natural Science Foundation of China 82325004National Natural Science Foundation of China 82370454National Natural Science Foundation of China 92168114Natural Science Foundation of Beijing Municipality 7252157Natural Science Foundation of Beijing Municipality F251013
6 · The paper itself

Abstract

Cardiac ischemia/reperfusion (I/R) injury is an important therapeutic target for ischemic heart disease. Lipid droplets (LDs) are the key organelles involved in lipid metabolism. This study aimed to identify the LD-mediated protection against lipotoxicity in cardiac I/R injury. LD accumulation is upregulated in hearts subjected to I/R injury; however, it is insufficient to neutralize lipotoxicity or prevent cardiomyocyte death. Seipin played a central role in LD biogenesis in cardiomyocytes following I/R injury. Seipin deficiency led to reduced LD levels and exacerbated cardiac I/R injury. Whereas increased LD levels, via Seipin overexpression or lipolysis inhibition, ameliorated myocardial I/R injury. I/R-induced downregulation of Seipin is attributed to the reduced expression of its transcription factor USF1, which is required for metabolic adaptation in acute myocardial ischemia. These findings not only elucidate the pathophysiological roles of LDs and Seipin but also provide a promising therapeutic target for myocardial I/R injury.

Indexed as

GTP-Binding Protein gamma SubunitsLipid DropletsMyocardial Reperfusion InjuryMyocytes, CardiacAnimalsDisease Models, AnimalLipid MetabolismMaleMiceMice, Inbred C57BLBscl2 protein, mouseGTP-Binding Protein gamma Subunitscardiomyocyte deathheartischemia/reperfusion injurylipid dropletseipin

Identifiers

PMID41255216
PMCPMC12866716

What Socratic holds

Textmetadata
LicenceCC BY
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.