ArticleCell death & disease2018
Inhibition of p53 prevents diabetic cardiomyopathy by preventing early-stage apoptosis and cell senescence, reduced glycolysis, and impaired angiogenesis.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 107 citations in OpenAlex.
- Cellular Senescence in Diabetic Cardiomyopathy: Mechanistic Insights and Therapeutic Perspectives.Cardiovascular drugs and therapy · 2026Review
- Global research trends of cell death in diabetic cardiomyopathy from 2000 to 2024: a bibliometric analysis and integrative overview.Journal of cardiothoracic surgery · 2026Review
- Review
- p53: from understanding its structure to advances in therapeutic targeting.Signal transduction and targeted therapy · 2026Review
- Microneedle Delivery of Small Extracellular Vesicles From Young Blood to Treat Endothelial Senescence.Advanced materials (Deerfield Beach, Fla.) · 2026Article
- Pathogenesis of diabetic cardiomyopathy and emerging therapeutic strategies: a network-based perspective.Frontiers in clinical diabetes and healthcare · 2026Review
- (Pro)renin receptor promotes cardiomyocyte senescence via tripartite motif-containing 24-mediated stabilization of p53 in diabetic cardiomyopathy.Acta biochimica et biophysica Sinica · 2025Article
- Right ventricular dysfunctions in type 1 diabetic mice: A longitudinal study.World journal of diabetes · 2025Article
- Inflammaging and Senescence-Driven Extracellular Matrix Remodeling in Age-Associated Cardiovascular Disease.Biomolecules · 2025Review
- The role of cellular senescence in cardiovascular disease.Cell death discovery · 2025Review
- High-intensity interval training (HIIT) ameliorates cardiac hypertrophy and fibrosis in diabetic rats: the role of P53 and SIRT1.Journal of molecular histology · 2025Article
- Aberrant activation of p53-TRIB3 axis contributes to diabetic myocardial insulin resistance and sulforaphane protection.Journal of advanced research · 2025Article
- Novel impact of metal ion-induced cell death on diabetic cardiomyopathy pathogenesis and therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- Tenascin-C drives cardiovascular dysfunction in a mouse model of diabetic cardiomyopathy.Cardiovascular diabetology · 2025Article
- Review
- Exercise in Diabetic Cardiomyopathy: Its Protective Effects and Molecular Mechanism.International journal of molecular sciences · 2025Review
- Research Hotspots and Frontier Trends of Autophagy in Diabetic Cardiomyopathy From 2014 to 2024: A Bibliometric Analysis.Journal of multidisciplinary healthcare · 2025Article
- Validation of Senescence of the Role of ATM/P53 Pathway in Myocardial Senescence in Mice with Sepsis.Infection and drug resistance · 2025Article
- Unraveling the Molecular Mechanisms of SIRT7 in Angiogenesis: Insights from Substrate Clues.International journal of molecular sciences · 2024Review
- Cellular Senescence: A Bridge Between Diabetes and Microangiopathy.Biomolecules · 2024Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated tumor suppressor p53 expression has been associated with heart diseases, including the diabetic heart. However, its precise role in the pathogenesis of diabetic cardiomyopathy (DCM) remains unclear. We hypothesized that the development of DCM is attributed to up-regulated p53-mediated both early cardiac cell death and persistent cell senescence, glycolytic and angiogenetic dysfunctions. The present study investigated the effect of p53 inhibition with its specific inhibitor pifithrin-α (PFT-α) on the pathogenesis of DCM and its associated mechanisms. Type 1 diabetes was induced with multiple low doses of streptozotocin. Both hyperglycemic and age-matched control mice were treated with and without PFT-α five times a week for 2 months and then sacrificed at 3 and 6 months post-diabetes. Treatment with PFT-α significantly prevented the progression of diabetes-induced cardiac remodeling and dysfunction (i.e., DCM). Mechanistically, the inhibition of p53 prevented the cardiac apoptosis during early-stage diabetes (0.5 month), attenuated diabetes-induced cell senescence (3 and 6 months), and improved both glycolytic and angiogenic defects by increasing hypoxia-induced factor (HIF)-1α protein stability and upregulating HIF-1α transcription of specific target genes at 3 and 6 months after diabetes. Therefore, the targeted inhibition of p53 in diabetic individuals may provide a novel approach for the prevention of DCM.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.