Evidence map›Paper›PMID 40290893›Full record

ArticleMaterials today. Bio2025

Ceria nanoparticles alleviate myocardial ischemia-reperfusion injury by inhibiting cardiomyocyte apoptosis via alleviating ROS mediated excessive mitochondrial fission.

Ying Sun, Jiabao Xu, Ling Zou, Yan Tan, Jie Li, Haoran Xin, Yanli Guo, Weikai Kong, Dingyuan Tian, Xinyu Bao and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Materials today. Bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

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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

15 authors.

Ying SunDepartment of Pathophysiology, College of High Altitude Military Medicine, Army Medical University, Chongqing, 400038, China.
Jiabao XuDepartment of Pathophysiology, College of High Altitude Military Medicine, Army Medical University, Chongqing, 400038, China.
Ling ZouSchool of Biomedical Engineering and Medical Imaging, Army Medical University, Chongqing, 400038, China.
Yan TanDepartment of Pathophysiology, College of High Altitude Military Medicine, Army Medical University, Chongqing, 400038, China.
Jie LiDepartment of Cardiovascular Medicine, Center for Circadian Metabolism and Cardiovascular Disease, Southwest Hospital, Army Medical University, Chongqing, 400038, China.
Haoran XinDepartment of Cardiovascular Medicine, Center for Circadian Metabolism and Cardiovascular Disease, Southwest Hospital, Army Medical University, Chongqing, 400038, China.
Yanli GuoDepartment of Ultrasound, Southwest Hospital, Army Medical University, Chongqing, 400038, China.
Weikai KongInstitute of Pathology and Southwest Cancer Center, Southwest Hospital, Army Medical University, Chongqing, 400038, China.
Dingyuan TianDepartment of Cardiovascular Medicine, Center for Circadian Metabolism and Cardiovascular Disease, Southwest Hospital, Army Medical University, Chongqing, 400038, China.
Xinyu BaoDepartment of Pathophysiology, College of High Altitude Military Medicine, Army Medical University, Chongqing, 400038, China.
Xiaoqin WanDepartment of Pathophysiology, College of High Altitude Military Medicine, Army Medical University, Chongqing, 400038, China.
Xiaoxu LiKey Laboratory of Extreme Environmental Medicine, Ministry of Education of China, Chongqing, 400038, China.
Zhihui ZhangDepartment of Cardiovascular Medicine, Center for Circadian Metabolism and Cardiovascular Disease, Southwest Hospital, Army Medical University, Chongqing, 400038, China.
Xiaochao YangSchool of Biomedical Engineering and Medical Imaging, Army Medical University, Chongqing, 400038, China.
Fang DengDepartment of Pathophysiology, College of High Altitude Military Medicine, Army Medical University, Chongqing, 400038, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reperfusion through thrombolytic therapy or primary percutaneous coronary intervention is commonly used to deal with acute myocardial infarction. However, the reperfusion procedure is accompanied by myocardial ischemia-reperfusion injury (MIRI). Currently, there is no therapeutics that can effectively deal with MIRI in clinical practice. Herein, the potential of ceria nanoparticles (CNPs) coated by different ligands in the treatment of rat MIRI is evaluated. The results demonstrate that CNPs can effectively modulate the oxidative stress in the heart tissue through the elimination of reactive oxygen species (ROS) and stimulation of endogenous antioxidant system. The inhibition of oxidative stress results in the reduction of p-Drp1 (Ser 616) which is critical in driving the fission and fragmentation of mitochondria. The improved mitochondrial dynamics saves the cardiomyocytes from apoptosis and reduces the acute injury of left ventricular wall during the MIRI. The ejection function of the left ventricle for both the short-term and long-term MIRI rats is well preserved. We therefore believe based on these results that the administration of CNPs is beneficial in the attenuation of MIRI during the acute stage. These findings provide useful information for the future fabrication of inorganic antioxidant nanomedicine for the treatment of MIRI.

Indexed as

Ceria nanoparticlesMitochondriaMyocardial ischemia-reperfusion injuryOxidative stressReactive oxygen species

Identifiers

PMID40290893
PMCPMC12033917

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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.