ArticleJournal of cardiovascular translational research2020
Involvement of p53 in the Responses of Cardiac Muscle Cells to Heat Shock Exposure and Heat Acclimation.
Article in Journal of cardiovascular translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
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Who cites it
2 citing papers in PubMed, 5 citations in OpenAlex.
- Article
- Cytosolic p53 Inhibits Parkin-Mediated Mitophagy and Promotes Acute Liver Injury Induced by Heat Stroke.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intense heat stress induces damage to the heart, whereas mild to moderate heat stress protects the heart against subsequent ischemic injury. The mechanisms underlying the detrimental and beneficial effects of heat stress remain unclear. In this study, we investigated the role of p53 in the responses of cardiac muscle cells to acute heat exposure and heat acclimation (HA). Heat exposure increased the levels of caspase and annexin, and levels of cytosolic, nuclear, and mitochondrial p53 protein in H9c2 cells. Pifithrin-α or pifithrin-μ reduced heat-induced apoptotic response in these cells. HA reduced localization of p53 in the mitochondria and improved cell viability during heat exposure. The effects of heat exposure and HA on p53 were further verified in vivo in mouse heart tissue. These results suggest that p53 plays a role in heat-induced apoptosis in cardiac muscle cells. The protective effect of HA against heat injury likely involves a p53-dependent mechanism.
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