ReviewCells2020
Metabolic Dysfunction in Hutchinson-Gilford Progeria Syndrome.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 45 citations in OpenAlex.
- Lonafarnib clinical trials demonstrate uncoupling of the muscle-bone unit in Hutchinson-Gilford Progeria Syndrome.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 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
- Rare case of longevity in Hutchinson-Gilford progeria syndrome and literature review.Orphanet journal of rare diseases · 2025Review
- Disease pathogenicity in Hutchinson-Gilford progeria syndrome mice: insights from lung-associated alterations.Molecular medicine (Cambridge, Mass.) · 2025Article
- MAM-STAT3-Driven Mitochondrial CaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cardiac and skeletal muscle manifestations in the G608G mouse model of Hutchinson-Gilford progeria syndrome.Aging cell · 2024Article
- Premature aging effects on COVID-19 pathogenesis: new insights from mouse models.Scientific reports · 2024Article
- Mitophagy defect mediates the aging-associated hallmarks in Hutchinson-Gilford progeria syndrome.Aging cell · 2024Article
- The Use of Peripheral Nerve Block and Intra-articular Steroid Injection for Pain Management in an Adolescent with Hutchinson-Gilford Progeria Syndrome: A Case Report.Acta medica Philippina · 2024Article
- Article
- [Wiedemann-Rautenstrauch syndrome. The first description of a clinical case in the Russian Federation].Problemy endokrinologii · 2023Article
- Inflammation and aging: signaling pathways and intervention therapies.Signal transduction and targeted therapy · 2023Review
- Medial Sclerosis-Epidemiology and Clinical Significance.Deutsches Arzteblatt international · 2023Review
- Native lamin A/C proteomes and novel partners from heart and skeletal muscle in a mouse chronic inflammation model of human frailty.Frontiers in cell and developmental biology · 2023Article
- STAT1 Drives the Interferon-Like Response and Aging Hallmarks in Progeria.Aging biology · 2023Article
- Lysophosphatidic Acid Receptor 3 Promotes Mitochondrial Homeostasis against Oxidative Stress: Potential Therapeutic Approaches for Hutchinson-Gilford Progeria Syndrome.Antioxidants (Basel, Switzerland) · 2022Article
- Nuclear Envelope Integrity in Health and Disease: Consequences on Genome Instability and Inflammation.International journal of molecular sciences · 2021Review
- Long-term survival in a patient with Hutchinson-Gilford progeria syndrome and osteosarcoma: A case report.World journal of clinical cases · 2021Article
- Directly Reprogrammed Human Neurons to Understand Age-Related Energy Metabolism Impairment and Mitochondrial Dysfunction in Healthy Aging and Neurodegeneration.Oxidative medicine and cellular longevity · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Hutchinson-Gilford Progeria Syndrome (HGPS) is a segmental premature aging disease causing patient death by early teenage years from cardiovascular dysfunction. Although HGPS does not totally recapitulate normal aging, it does harbor many similarities to the normal aging process, with patients also developing cardiovascular disease, alopecia, bone and joint abnormalities, and adipose changes. It is unsurprising, then, that as physicians and scientists have searched for treatments for HGPS, they have targeted many pathways known to be involved in normal aging, including inflammation, DNA damage, epigenetic changes, and stem cell exhaustion. Although less studied at a mechanistic level, severe metabolic problems are observed in HGPS patients. Interestingly, new research in animal models of HGPS has demonstrated impressive lifespan improvements secondary to metabolic interventions. As such, further understanding metabolism, its contribution to HGPS, and its therapeutic potential has far-reaching ramifications for this disease still lacking a robust treatment strategy.
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.