ArticleScientific reports2020
Human pluripotent stem cell-based models suggest preadipocyte senescence as a possible cause of metabolic complications of Werner and Bloom Syndromes.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 17 citations in OpenAlex.
- Bloom Syndrome Presenting as Early-Onset Bilateral Breast Cancer and Multisystem Metabolic Disease: A Case Report.Cureus · 2026Article
- Novel Homozygous Variants in CIDEC and WRN in a Young Female with Lipodystrophy and Thyroid Cancer.International journal of molecular sciences · 2026Article
- The role of cellular senescence in ovarian aging.npj aging · 2024Review
- WRN loss accelerates abnormal adipocyte metabolism in Werner syndrome.Cell & bioscience · 2024Article
- Senescence-associated inflammation and inhibition of adipogenesis in subcutaneous fat in Werner syndrome.Aging · 2023Article
- Article
- Lipodystrophy-associated progeroid syndromes.Hormones (Athens, Greece) · 2022Review
- DNA repair-related genes and adipogenesis: Lessons from congenital lipodystrophies.Genetics and molecular biology · 2022Article
- Molecular and Cellular Bases of Lipodystrophy Syndromes.Frontiers in endocrinology · 2021Review
- Application of human iPSC-derived white, beige, and brown adipocytes for metabolic disease modeling and transplantation therapy.Cell transplantationReview
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Werner Syndrome (WS) and Bloom Syndrome (BS) are disorders of DNA damage repair caused by biallelic disruption of the WRN or BLM DNA helicases respectively. Both are commonly associated with insulin resistant diabetes, usually accompanied by dyslipidemia and fatty liver, as seen in lipodystrophies. In keeping with this, progressive reduction of subcutaneous adipose tissue is commonly observed. To interrogate the underlying cause of adipose tissue dysfunction in these syndromes, CRISPR/Cas9 genome editing was used to generate human pluripotent stem cell (hPSC) lacking either functional WRN or BLM helicase. No deleterious effects were observed in WRN
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Registered trials
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