ArticleCell death & disease2019
Ser46 phosphorylation of p53 is an essential event in prolyl-isomerase Pin1-mediated p53-independent apoptosis in response to heat stress.
Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 45 citations in OpenAlex.
- Article
- Heat stroke and the liver: mechanisms of injury and therapeutic strategies.European journal of medical research · 2026Review
- The synergistic effects of linalool and chitosan-carbon nanotubes enhance the healing of infectious wounds.Scientific reports · 2025Article
- A Novel Mechanism of the p53 Isoform Δ40p53α in Regulating Collagen III Expression in TGFβ1-Induced LX-2 Human Hepatic Stellate Cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- The pathogenesis and management of heatstroke and heatstroke-induced lung injury.Burns & trauma · 2025Review
- The mechanism by which FGF23/FGFR-1 activates NOX2-ROS in vascular endothelial cells in the context of severe heat stroke-induced acute lung injury.Burns & trauma · 2025Article
- Butyrolactone-I from Marine Fungal Metabolites Mitigates Heat-Stress-Induced Apoptosis in IPEC-J2 Cells and Mice Through the ROS/PERK/CHOP Signaling Pathway.Marine drugs · 2024Article
- The mechanisms behind heatstroke-induced intestinal damage.Cell death discovery · 2024Review
- Unraveling the role of long non-coding RNAs in chronic heat stress-induced muscle injury in broilers.Journal of animal science and biotechnology · 2024Article
- The significant mechanism and treatments of cell death in heatstroke.Apoptosis : an international journal on programmed cell death · 2024Review
- Expression and role of FKBPL in lung adenocarcinoma.Journal of Cancer · 2024Article
- Review
- Heat stress combined with lipopolysaccharide induces pulmonary microvascular endothelial cell glycocalyx inflammatory damage in vitro.Immunity, inflammation and disease · 2023Article
- Cell cycle-specific phosphorylation of p53 protein in A549 cells exposed to cisplatin and standardized air pollutants.Frontiers in physiology · 2023Article
- The regulatory role of Pin1 in neuronal death.Neural regeneration research · 2023Review
- Red Algae “Sarcodia suieae” Acetyl-Xylogalactan Downregulate Heat-Induced Macrophage Stress Factors Ddit3 and Hyou1 Compared to the Aquatic Animal Model of Nile Tilapia (Oreochromis niloticus) Brain Arachidonic Acid ExpressionInternational journal of molecular sciences · 2022Article
- Elevation of effective p53 expression sensitizes wild-type p53 breast cancer cells to CDK7 inhibitor THZ1.Cell communication and signaling : CCS · 2022Article
- PIN1-mediated ROS production is involved in antagonism of N-acetyl-L-cysteine against arsenic-induced hepatotoxicity.Toxicology research · 2022Article
- Review
- A bibliometric analysis of PIN1 and cell death.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heat stroke has increased in frequency worldwide in recent years and continues to have a high morbidity and mortality. Identification of the mechanisms mediating heat stoke is important and necessary. Our preliminary study revealed heat stress (HS)-induced apoptosis of vascular endothelial cells was associated with reactive oxygen species (ROS)-induced p53 translocation into mitochondria. Previous studies have suggested the prolyl-isomerase Pin1 regulates p53 functioning through specific binding to p53 phosphorylation sites. Based on these studies, we presumed Pin1 is a key intermediate in regulation of mitochondrial p53 translocation through a HS-induced ROS-p53 transcription-independent apoptosis pathway. In this context, we revealed p53 had a crucial role in a HS-induced mitochondrial apoptotic pathway, where p53 protein rapidly translocated into mitochondria in endothelial cells both in vitro and in vivo. In particular, HS caused an increase in p53 phosphorylation at Ser46 that facilitated interactions with phosphorylation-dependent prolyl-isomerase Pin1, which has a key role in promoting HS-induced localization of p53 to mitochondria. Furthermore, we also found ROS production was a critical mediator in HS-induced Pin1/p53 signaling and was involved in regulating mitochondrial apoptosis pathway activation. Therefore, we have contributed to our profound understanding of the mechanism underlying HS-induced endothelial dysfunction in an effort to reduce the mortality and morbidity of heat stroke.
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