ArticleAging cell2018
Targeting the phospholipase A2 receptor ameliorates premature aging phenotypes.
Article in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
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
21 citing papers in PubMed, 39 citations in OpenAlex.
- The proteogenomic landscape of the human kidney and implications for cardio-kidney-metabolic health.Nature medicine · 2025 · on this mapArticle
- Article
- CD133Nature aging · 2023Article
- Loss of Pla2r1 decreases cellular senescence and age-related alterations caused by aging and Western diets.Aging cell · 2023Article
- Convergent genomics of longevity in rockfishes highlights the genetics of human life span variation.Science advances · 2023Article
- Urinary PART1 and PLA2R1 Could Potentially Serve as Diagnostic Markers for Diabetic Kidney Disease Patients.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- PEDF Deletion Induces Senescence and Defects in Phagocytosis in the RPE.International journal of molecular sciences · 2022Article
- Identification of molecular mechanism and key biomarkers in membranous nephropathy by bioinformatics analysis.American journal of translational research · 2022Article
- Neuroprotective Potential of Ellagic Acid: A Critical Review.Advances in nutrition (Bethesda, Md.) · 2021Review
- Review
- PLA2R1 promotes DNA damage and inhibits spontaneous tumor formation during aging.Cell death & disease · 2021Article
- Exploring the Differences in Molecular Mechanisms and Key Biomarkers Between Membranous Nephropathy and Lupus Nephritis Using Integrated Bioinformatics Analysis.Frontiers in genetics · 2021Article
- Progress and trends in the development of therapies for Hutchinson-Gilford progeria syndrome.Aging cell · 2020Review
- Observational
- Chemical Proteomic Profiling of the Interacting Proteins of Isoprenoid Pyrophosphates.Analytical chemistry · 2020Article
- Single-Nucleotide Polymorphisms (SNPs) Both Associated with Hypertension and Contributing to Accelerated-Senescence Traits in OXYS Rats.International journal of molecular sciences · 2020Article
- The JAK1/2 inhibitor ruxolitinib delays premature aging phenotypes.Aging cell · 2020Article
- Pharmacotherapy to gene editing: potential therapeutic approaches for Hutchinson-Gilford progeria syndrome.GeroScience · 2020Review
- The Potential Role of Regulatory B Cells in Idiopathic Membranous Nephropathy.Journal of immunology research · 2020Review
- The role of lipid metabolism in aging, lifespan regulation, and age-related disease.Aging cell · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is a lethal premature aging that recapitulates many normal aging characteristics. This disorder is caused by mutation in the LMNA gene leading to the production of progerin which induces misshapen nuclei, cellular senescence, and aging. We previously showed that the phospholipase A2 receptor (PLA2R1) promotes senescence induced by replicative, oxidative, and oncogenic stress but its role during progerin-induced senescence and in progeria is currently unknown. Here, we show that knockdown of PLA2R1 prevented senescence induced by progerin expression in human fibroblasts and markedly delayed senescence of HGPS patient-derived fibroblasts. Whole-body knockout of Pla2r1 in a mouse model of progeria decreased some premature aging phenotypes, such as rib fracture and decreased bone content, together with decreased senescence marker. Progerin-expressing human fibroblasts exhibited a high frequency of misshapen nuclei and increased farnesyl diphosphate synthase (FDPS) expression compared to controls; knockdown of PLA2R1 reduced the frequency of misshapen nuclei and normalized FDPS expression. Pamidronate, a FDPS inhibitor, also reduced senescence and misshapen nuclei. Downstream of PLA2R1, we found that p53 mediated the progerin-induced increase in FDPS expression and in misshapen nuclei. These results suggest that PLA2R1 mediates key premature aging phenotypes through a p53/FDPS pathway and might be a new therapeutic target.
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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.