ArticleCells2020
Progerin Expression Induces Inflammation, Oxidative Stress and Senescence in Human Coronary Endothelial Cells.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 69 citations in OpenAlex.
- Transcriptional profiling of Hutchinson-Gilford progeria patients identifies primary target pathways of progerin.Nucleus (Austin, Tex.) · 2026Article
- The unfolded protein response in progeria arteries originates from non-endothelial cell types.Life science alliance · 2026Article
- Baricitinib Augments Lonafarnib Therapy to Preserve Colonic Homeostasis and Microbial Balance in a Mouse Model of Progeria.Aging cell · 2025Article
- Nuclear envelope components in vascular mechanotransduction: emerging roles in vascular health and disease.Nucleus (Austin, Tex.) · 2025Review
- Reduced ZMPSTE24 expression leads to prelamin accumulation and development of steatosis in MASLD patients.Scientific reports · 2025Article
- Microhand Platform Equipped with Plate-Shaped End-Effectors Enables Precise Probing of Intracellular Structure Contribution to Whole-Cell Mechanical Properties.Micromachines · 2025Article
- Progerin regulates actin cytoskeletal remodeling and inhibits EMT and metastasis in triple‑negative breast cancer cells.International journal of oncology · 2025Article
- The role of cellular senescence in cardiovascular disease.Cell death discovery · 2025Review
- Transcriptional profiling of Hutchinson-Gilford Progeria patients identifies primary target pathways of progerin.bioRxiv : the preprint server for biology · 2025Article
- Impaired stemness in aging periodontal ligament stem cells is mediated by the progerin/endoplasmic reticulum stress/p53 axis.Journal of advanced research · 2025Article
- How to measure and model cardiovascular aging.Cardiovascular research · 2025Review
- Impact of miR-181a on SIRT1 Expression and Senescence in Hutchinson-Gilford Progeria Syndrome.Diseases (Basel, Switzerland) · 2025Article
- C-C chemokine ligand 5 from women subcutaneous adipose tissue has a central role in vascular aging.Cardiovascular diabetology · 2025Article
- Progerin mRNA Is Associated with Smoking and Signs of Increased Microvascular Damage in Patients with Diabetic Macular Edema.International journal of molecular sciences · 2025Article
- Article
- Endothelial cell-specific progerin expression does not cause cardiovascular alterations and premature death.Aging cell · 2025Article
- Angiopoietin-2: A Therapeutic Target for Vascular Protection in Hutchinson-Gilford Progeria Syndrome.International journal of molecular sciences · 2024Review
- A defective splicing machinery promotes senescence through MDM4 alternative splicing.Aging cell · 2024Article
- Endothelial YAP/TAZ activation promotes atherosclerosis in a mouse model of Hutchinson-Gilford progeria syndrome.The Journal of clinical investigation · 2024Article
- Senescent endothelial cells promote pathogenic neutrophil trafficking in inflamed tissues.EMBO reports · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is a rare premature aging disorder notably characterized by precocious and deadly atherosclerosis. Almost 90% of HGPS patients carry a LMNA p.G608G splice variant that leads to the expression of a permanently farnesylated abnormal form of prelamin-A, referred to as progerin. Endothelial dysfunction is a key determinant of atherosclerosis, notably during aging. Previous studies have shown that progerin accumulates in HGPS patients' endothelial cells but also during vascular physiological aging. However, whether progerin expression in human endothelial cells can recapitulate features of endothelial dysfunction is currently unknown. Herein, we evaluated the direct impact of exogenously expressed progerin and wild-type lamin-A on human endothelial cell function and senescence. Our data demonstrate that progerin, but not wild-type lamin-A, overexpression induces endothelial cell dysfunction, characterized by increased inflammation and oxidative stress together with persistent DNA damage, increased cell cycle arrest protein expression and cellular senescence. Inhibition of progerin prenylation using a pravastatin-zoledronate combination partly prevents these defects. Our data suggest a direct proatherogenic role of progerin in human endothelial cells, which could contribute to HGPS-associated early atherosclerosis and also potentially be involved in physiological endothelial aging participating to age-related cardiometabolic diseases.
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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.