Evidence map›Paper›PMID 31502361›Full record

ArticleJournal of cellular and molecular medicine2019

MCU Up-regulation contributes to myocardial ischemia-reperfusion Injury through calpain/OPA-1-mediated mitochondrial fusion/mitophagy Inhibition.

Lichun Guan, Zhimei Che, Xiangdong Meng, Yong Yu, Minghui Li, Ziqin Yu, Hui Shi, Dicheng Yang, Min Yu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% of its field
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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

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  14. Role of mitochondrial CaMolecular medicine reports · 2025
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16 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

Lichun GuanDepartment of Cardiovascular Surgery, Shanghai General Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
Zhimei CheDepartment of Anesthesiology, Renji Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
Xiangdong MengDepartment of Cardiovascular Surgery, Shanghai General Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
Yong YuDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai Shi, China.
Minghui LiDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai Shi, China.
Ziqin YuDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai Shi, China.
Hui ShiDepartment of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai Shi, China.
Dicheng YangDepartment of Cardiovascular Surgery, Shanghai General Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
Min YuDepartment of Cardiovascular Surgery, Shanghai General Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.ORCID 0000-0002-0042-2196
Shanghai Jiao Tong University · CNFudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial dynamic disorder is involved in myocardial ischemia/reperfusion (I/R) injury. To explore the effect of mitochondrial calcium uniporter (MCU) on mitochondrial dynamic imbalance under I/R and its related signal pathways, a mouse myocardial I/R model and hypoxia/reoxygenation model of mouse cardiomyocytes were established. The expression of MCU during I/R increased and related to myocardial injury, enhancement of mitochondrial fission, inhibition of mitochondrial fusion and mitophagy. Suppressing MCU functions by Ru360 during I/R could reduce myocardial infarction area and cardiomyocyte apoptosis, alleviate mitochondrial fission and restore mitochondrial fusion and mitophagy. However, spermine administration, which could enhance MCU function, deteriorated the above-mentioned myocardial cell injury and mitochondrial dynamic imbalanced. In addition, up-regulation of MCU promoted the expression and activation of calpain-1/2 and down-regulated the expression of Optic atrophy type 1 (OPA1). Meantime, in transgenic mice (overexpression calpastatin, the endogenous inhibitor of calpain) I/R model and OPA1 knock-down cultured cell. In I/R models of transgenic mice over-expressing calpastatin, which is the endogenous inhibitor of calpain, and in H/R models with siOPA1 transfection, inhibition of calpains could enhance mitochondrial fusion and mitophagy, and inhibit excessive mitochondrion fission and apoptosis through OPA1. Therefore, we conclude that during I/R, MCU up-regulation induces calpain activation, which down-regulates OPA1, consequently leading to mitochondrial dynamic imbalance.

Indexed as

Mitochondrial DynamicsMitophagyUp-RegulationAdenosine TriphosphateAnimalsAnimals, NewbornApoptosisCalcium-Binding ProteinsCalcium ChannelsCalpainEnzyme InhibitorsGTP PhosphohydrolasesHomeostasisMaleMice, Inbred C57BLMice, TransgenicAdenosine TriphosphateCalcium-Binding ProteinsCalcium ChannelsCalpaincalpastatinEnzyme InhibitorsGTP Phosphohydrolasesmitochondrial calcium uniporterOpa1 protein, mouseProtective Agentscalpainischemia/reperfusion (I/R)mitochondrial calcium uniporter (MCU)mitochondrial fissionmitophagy

Identifiers

PMID31502361
PMCPMC6815825
OpenAlexW2972338699

What OpenQuestion 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 OpenQuestion graph.