ArticleAging cell2019
Doubled lifespan and patient-like pathologies in progeria mice fed high-fat diet.
Article in Aging cell, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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.
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Who cites it
27 citing papers in PubMed, 39 citations in OpenAlex.
- Mutation-agnostic base editing of the progerin farnesylation site rescues Hutchinson-Gilford progeria syndrome phenotypes in neuromuscular organoids.Nature communications · 2026Article
- Activation of the Lactate Receptor GPR81 Ameliorates Senescence Hallmarks and Improves Muscle Function in Cellular and Progeroid Models of Aging.Aging cell · 2026Article
- Metabolic Dysregulation in Laminopathies: Implications for Heart Failure and Cardiac Health.Current heart failure reports · 2026Review
- A study on the nutritional status and body composition of children with Hutchinson-Gilford progeria syndrome.Orphanet journal of rare diseases · 2026Article
- Sterile inflammation in laminopathies.European journal of cell biology · 2025Review
- Baricitinib Augments Lonafarnib Therapy to Preserve Colonic Homeostasis and Microbial Balance in a Mouse Model of Progeria.Aging cell · 2025Article
- Disease pathogenicity in Hutchinson-Gilford progeria syndrome mice: insights from lung-associated alterations.Molecular medicine (Cambridge, Mass.) · 2025Article
- Nuclear envelope budding inhibition slows down progerin-induced aging process.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Senescent endothelial cells promote pathogenic neutrophil trafficking in inflamed tissues.EMBO reports · 2024Article
- Biomechanical and transcriptional evidence that smooth muscle cell death drives an osteochondrogenic phenotype and severe proximal vascular disease in progeria.Biomechanics and modeling in mechanobiology · 2023Article
- Hepatic hydrogen sulfide levels are reduced in mouse model of Hutchinson-Gilford progeria syndrome.Aging · 2023Article
- Article
- Smooth Muscle Cell Death Drives an Osteochondrogenic Phenotype and Severe Proximal Vascular Disease in Progeria.bioRxiv : the preprint server for biology · 2023Article
- STAT1 Drives the Interferon-Like Response and Aging Hallmarks in Progeria.Aging biology · 2023Article
- In vivo stress reporters as early biomarkers of the cellular changes associated with progeria.Journal of cellular and molecular medicine · 2022Article
- Preclinical Advances of Therapies for Laminopathies.Journal of clinical medicine · 2021Review
- Gene-by-environment modulation of lifespan and weight gain in the murine BXD family.Nature metabolism · 2021Article
- Impact of Progerin Expression on Adipogenesis in Hutchinson-Gilford Progeria Skin-Derived Precursor Cells.Cells · 2021Article
- Article
- Paradoxical aortic stiffening and subsequent cardiac dysfunction in Hutchinson-Gilford progeria syndrome.Journal of the Royal Society, Interface · 2020Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Hutchinson-Gilford Progeria Syndrome (HGPS) is a devastating premature aging disease. Mouse models have been instrumental for understanding HGPS mechanisms and for testing therapies, which to date have had only marginal benefits in mice and patients. Barriers to developing effective therapies include the unknown etiology of progeria mice early death, seemingly unrelated to the reported atherosclerosis contributing to HGPS patient mortality, and mice not recapitulating the severity of human disease. Here, we show that progeria mice die from starvation and cachexia. Switching progeria mice approaching death from regular diet to high-fat diet (HFD) rescues early lethality and ameliorates morbidity. Critically, feeding the mice only HFD delays aging and nearly doubles lifespan, which is the greatest lifespan extension recorded in progeria mice. The extended lifespan allows for progeria mice to develop degenerative aging pathologies of a severity that emulates the human disease. We propose that starvation and cachexia greatly influence progeria phenotypes and that nutritional/nutraceutical strategies might help modulate disease progression. Importantly, progeria mice on HFD provide a more clinically relevant animal model to study mechanisms of HGPS pathology and to test therapies.
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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.