ArticleBiological trace element research2022
Protective Effect of Manganese on Apoptosis and Mitochondrial Function of Heat-Stressed Primary Chick Embryonic Myocardial Cells.
Article in Biological trace element research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 4 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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Quantitative Proteomics Reveals Manganese Alleviates Heat Stress of Broiler Myocardial Cells via Regulating Nucleic Acid Metabolism.Biological trace element research · 2024Article
- Vitexin Regulates Heat Shock Protein Expression by Modulating ROS Levels Thereby Protecting against Heat-Stress-Induced Apoptosis.Molecules (Basel, Switzerland) · 2023Article
- Protective Effect of Manganese on Apoptosis and Mitochondrial Function of Heat-Stressed Primary Chick Embryonic Myocardial Cells.Biological trace element research · 2022Article
- Trehalose Attenuates Oxidative Stress and Endoplasmic Reticulum Stress-Mediated Apoptosis in IPEC-J2 Cells Subjected to Heat Stress.Animals : an open access journal from MDPI · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Heat stress, as a kind of oxidative stress, induces cell apoptosis. Apoptosis is a form of programmed cell death, and mitochondria play an important role in apoptosis. Manganese (Mn) has an antioxidant capacity by enhancing the activity of manganese superoxide dismutase (MnSOD). To investigate the potential effect of Mn on heat stress-induced apoptosis and mitochondrial function, we examined crucial related factors in the context of heat stress using primary chick embryonic myocardial cells pretreated with Mn for 24 h. The results showed that Mn restored the heat stress-induced decrease in cell viability and reduced the activities of caspase-3 (P < 0.05). The repression of the Δψm and intracellular ATP content caused by heat stress was reversed dramatically in the Mn pretreatment group (P < 0.05). Additionally, Mn inhibited heat stress-induced mitochondrial fission, as shown by decreased mitochondrial fission-related protein dynamin-related protein 1 (Drp1) expression and increased mitochondrial fusion-related protein optic atrophy 1 (Opa1) and mitofusin 1 (Mfn1) (P < 0.05) in primary chick embryonic myocardial cells. It was concluded that Mn attenuates the mitochondrial-mediated apoptosis pathway and sustains mitochondrial structure and function under heat stress in primary chick embryonic myocardial cells.
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Registered trials
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