Evidence map›Paper›PMID 37565298›Full record

ArticleExperimental physiology2023

Loss and recovery of myocardial mitochondria in mice under different tail suspension time: Apoptosis and mitochondrial fission, fusion and autophagy.

Zhe Wang, Xing-Chen Wang, Ya-Fei Chen, Chuan-Li Wang, Le Chen, Ming-Yue Jiang, Xi-Wei Liu, Xiao-Xuan Zhang, Yong-Zhen Feng, Jin-Hui Xu

Open access · diamondAbstract read
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Article in Experimental physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

5 citing papers in PubMed, 9 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Zhe WangCollege of Life Sciences, Qufu Normal University, Qufu, Shandong, China.ORCID 0000-0002-4950-9954
Xing-Chen WangCollege of Life Sciences, Qufu Normal University, Qufu, Shandong, China.
Ya-Fei ChenCollege of Life Sciences, Qufu Normal University, Qufu, Shandong, China.
Chuan-Li WangCollege of Life Sciences, Qufu Normal University, Qufu, Shandong, China.
Le ChenCollege of Life Sciences, Qufu Normal University, Qufu, Shandong, China.
Ming-Yue JiangCollege of Life Sciences, Qufu Normal University, Qufu, Shandong, China.
Xi-Wei LiuCollege of Life Sciences, Qufu Normal University, Qufu, Shandong, China.
Xiao-Xuan ZhangCollege of Life Sciences, Qufu Normal University, Qufu, Shandong, China.
Yong-Zhen FengCollege of Life Sciences, Qufu Normal University, Qufu, Shandong, China.
Jin-Hui XuCollege of Life Sciences, Qufu Normal University, Qufu, Shandong, China.
Qufu Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long-term weightlessness in animals can cause changes in myocardial structure and function, in which mitochondria play an important role. Here, a tail suspension (TS) Kunming mouse (Mus musculus) model was used to simulate the effects of weightlessness on the heart. We investigated the effects of 2 and 4 weeks of TS (TS2 and TS4) on myocardial mitochondrial ultrastructure and oxidative respiratory function and on the molecular mechanisms of apoptosis and mitochondrial fission, autophagy and fusion-related signalling. Our study revealed significant changes in the ultrastructural features of cardiomyocytes in response to TS. The results showed: (1) mitochondrial swelling and disruption of cristae in TS2, but mitochondrial recovery and denser cristae in TS4; (2) an increase in the total number of mitochondria and number of sub-mitochondria in TS4; (3) no significant changes in the nuclear ultrastructure or DNA fragmentation among the two TS groups and the control group; (4) an increase in the bax/bcl-2 protein levels in the two TS groups, indicating increased activation of the bax-mediated apoptosis pathway; (5) no change in the phosphorylation ratio of dynamin-related protein 1 in the two TS groups; (6) an increase in the protein levels of optic atrophy 1 and mitofusin 2 in the two TS groups; and (7) in comparison to the TS2 group, an increase in the phosphorylation ratio of parkin and the ratio of LC3II to LC3I in TS4, suggesting an increase in autophagy. Taken together, these findings suggest that mitochondrial autophagy and fusion levels increased after 4 weeks of TS, leading to a restoration of the bax-mediated myocardial apoptosis pathway observed after 2 weeks of TS. NEW

findingsWhat is the central question of this study? What are the effects of 2 and 4 weeks of tail suspension on myocardial mitochondrial ultrastructure and oxidative respiratory function and on the molecular mechanisms of apoptosis and mitochondrial fission, autophagy and fusion-related signalling? What is the main finding and its importance? Increased mitochondrial autophagy and fusion levels after 4 weeks of tail suspension help to reshape the morphology and increase the number of myocardial mitochondria.

Indexed as

Hindlimb SuspensionMitochondria, HeartAnimalsApoptosisAutophagybcl-2-Associated X ProteinMiceMitochondrial DynamicsMyocytes, Cardiacbcl-2-Associated X Proteinapoptosisheartmicrogravitymitochondria

Identifiers

PMID37565298
PMCPMC10988507
OpenAlexW4385751422

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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.