ArticleNature medicine2009
A crucial role for adipose tissue p53 in the regulation of insulin resistance.
Article in Nature medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 496 papers, 1 of them a synthesis that pooled it.
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
496 citing papers in PubMed, 1 synthesis or guideline pooled it, 870 citations in OpenAlex.
- Pooled it
- Fasting-mimicking diet causes hepatic and blood markers changes indicating reduced biological age and disease risk.Nature communications · 2024Trial
- Lack of receptor for advanced glycation end products attenuates obesity-induced adipose tissue senescence in mice.Adipocyte · 2026Article
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- Human β-Cell Dedifferentiation and Diabetes.Journal of diabetes · 2026Review
- The vicious cycle of SASP and inflammaging promotes aging and age-related diseases.Communications biology · 2026Review
- Quantum and nanoscale sensing of microinflammation for earlier detection of chronic inflammatory and neuroimmune disease.Discover nano · 2026Review
- AAV-mediated FGF21 gene therapy promotes health span extension by whole-body tissue-specific adaptations.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Cellular Senescence and Aging: Mechanisms, Disease Convergence, and Therapeutic Frontiers.MedComm · 2026Review
- Adipocyte-specific ablation of Gadd45b exacerbates obesity-associated cellular senescence and metabolic disorders via Fgf1b promoter hypermethylation.Cell death and differentiation · 2026Article
- Chronic High-Fat Diet Does Not Alter Overall Cancer Incidence in Trp53R270H/+ Mice.Cancer research communications · 2026Article
- Natural senolytic activity ofiScience · 2026Article
- Senolytic treatment with dasatinib and quercetin selectively improves cardiac autonomic balance in obesity.GeroScience · 2026Article
- Cancer cachexia induces senescent reprogramming of brown adipose tissue and pro-cachectic S100A9 secretion by adipocytes.Cell death & disease · 2026Article
- 'Glucocorticoids, Cushing's syndrome and cellular senescence: a mechanistic link to metabolic ageing'.Endocrine connections · 2026Review
- p53: from understanding its structure to advances in therapeutic targeting.Signal transduction and targeted therapy · 2026Review
- Adipose Tissue Aging and Natural Interventions: Potential Roles of Polyphenols and Polysaccharides.Nutrients · 2026Review
- Sexual Dimorphism in the Initial Apoptotic Switch During MASH Progression in Mice.International journal of molecular sciences · 2026Article
- Context-Dependent Roles of ANGPTL2-Mediated Inflammaging in Tissue Homeostasis, Pathological Tissue Remodeling, and Longevity.Aging cell · 2026Article
- Insulin Resistance and Inflammation.International journal of molecular sciences · 2026Review
436 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various stimuli, such as telomere dysfunction and oxidative stress, can induce irreversible cell growth arrest, which is termed 'cellular senescence'. This response is controlled by tumor suppressor proteins such as p53 and pRb. There is also evidence that senescent cells promote changes related to aging or age-related diseases. Here we show that p53 expression in adipose tissue is crucially involved in the development of insulin resistance, which underlies age-related cardiovascular and metabolic disorders. We found that excessive calorie intake led to the accumulation of oxidative stress in the adipose tissue of mice with type 2 diabetes-like disease and promoted senescence-like changes, such as increased activity of senescence-associated beta-galactosidase, increased expression of p53 and increased production of proinflammatory cytokines. Inhibition of p53 activity in adipose tissue markedly ameliorated these senescence-like changes, decreased the expression of proinflammatory cytokines and improved insulin resistance in mice with type 2 diabetes-like disease. Conversely, upregulation of p53 in adipose tissue caused an inflammatory response that led to insulin resistance. Adipose tissue from individuals with diabetes also showed senescence-like features. Our results show a previously unappreciated role of adipose tissue p53 expression in the regulation of insulin resistance and suggest that cellular aging signals in adipose tissue could be a new target for the treatment of diabetes (pages 996-967).
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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.