ArticlePloS one2017
Ubiquinol-cytochrome c reductase core protein 1 may be involved in delayed cardioprotection from preconditioning induced by diazoxide.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Ubiquinol-cytochrome c reductase core protein 1 contributes to cardiac tolerance to acute exhaustive exercise.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Critical role of UQCRC1 in embryo survival, brain ischemic tolerance and normal cognition in mice.Cellular and molecular life sciences : CMLS · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to use long-term diazoxide treatment to establish a loss-of-cardioprotection model and then perform proteomics analysis to explore which proteins of mitochondrial inner membrane (MIM) are potentially involved in delayed cardioprotection. Rats received 1 to 8 weeks of diazoxide treatments (20 mg•kg-1•d-1) to establish a loss-of-cardioprotection model in different groups. Detection of serum cTnI levels and cell apoptosis assays in heart tissue were performed. Then, rats MIM after 0, 4 and 6 weeks of diazoxide treatment was isolated and proteomics analysis was performed. An invitro model of H9C2 cells was performed to explore the effects of targeted protein on delayed cardioprotection. The effect of delayed cardioprotection by diazoxide preconditioning disappeared when diazoxide treatments were given for six weeks or longer. Ubiquinol-cytochrome c reductase core protein 1 (UQCRC1) was identified in the proteomics analysis. UQCRC1 expression was upregulated by diazoxide treatment in H9C2 cells, and UQCRC1 down-regulation could increase the lactate dehydrogenase release and apoptosis rate after injury induced by oxygen glucose deprivation. These results showed that UQCRC1 might contribute to the loss-of-cardioprotection model induced by long-term diazoxide treatment and play a role in delayed cardioprotection.
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Registered trials
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