ArticleFood chemistry: X2023
Morphological changes of mitochondria-related to apoptosis during postmortem aging of beef muscles.
Article in Food chemistry: X, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
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.
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Who cites it
3 citing papers in PubMed, 11 citations in OpenAlex.
- The Molecular Mechanism of a Complex1-induced Apoptosis in Cancer Cells of the Esophagus.Current molecular medicine · 2026Article
- Monitoring early micro-oxidation under refrigeration: iron and oxidative markers predict quality loss in grass carp.Current research in food science · 2026Article
- Effect of mitochondrial calcium homeostasis-mediated endogenous enzyme activation on tenderness of beef muscle based on MCU modulators.Food chemistry: X · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate how postmortem muscle cells' mitochondria changed in morphology from three aspects: the outer membrane, cristae, and fission/fusion. Atomic force microscopy (AFM) results showed that mitochondria underwent a morphology transformation from normal to swelling and collapse. Meanwhile, the cleavage of OPA1, upregulation of OMA1, downregulation of Mic60 and transmission electron microscope micrographs revealed that mitochondrial cristae ruptured with an aging time extended. Additionally, the increased expressions of Fis1 and Drp1, and the AFM topographic images mutually confirmed mitochondrial fission. These results further proved from the perspective of mitochondrial morphology that the degree of mitochondrial damage increased with the postmortem aging time extended, which was consistent with the results of the release of cytochrome
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Registered trials
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