ArticleEuropean heart journal2021
Telomerase therapy reverses vascular senescence and extends lifespan in progeria mice.
Article in European heart journal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 88 citations in OpenAlex.
- Helpful to Live Healthier? Intermittent Hypoxic/Ischemic Training Benefits Vascular Homeostasis and Lipid Metabolism with Activating SIRT1 Pathways in Overweight/Obese Individuals.Obesity facts · 2024Trial
- MTR4: A Conserved Youth Factor for Vascular Endothelium.Aging cell · 2026Article
- Nanomedicine beyond carriers - devices, cells & living therapeutics.Biomedical microdevices · 2026Review
- Cellular Senescence and Aging: Mechanisms, Disease Convergence, and Therapeutic Frontiers.MedComm · 2026Review
- Telomerase is induced during wound healing across species.Skin health and disease · 2026Article
- Vascular Aging.Circulation · 2026Review
- mRNA medicine for cardiovascular disease.Nature cardiovascular research · 2026Review
- Telomerase Knockout in Myeloid Cells Predisposes Mice to Foam Cell Formation, Dyslipidemia, Lung Fibrosis, and Cardiac Dysfunction.Aging cell · 2026Article
- Telomerase mRNA-Lipid nanoparticles attenuate neuroinflammation after traumatic brain injury in mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Senescence-inhibitory Δ133p53α counteracts accelerated ageing and mortality.bioRxiv : the preprint server for biology · 2026Article
- The unfolded protein response in progeria arteries originates from non-endothelial cell types.Life science alliance · 2026Article
- Telomerase mRNA therapy protects human skin against radiation-induced DNA damage.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Protective effect and mechanism of SIRT1 under stress-induced vascular senescence.Open life sciences · 2026Review
- Grip strength as a systems biomarker of aging: neuromuscular junction constraints and biomarker decoupling in gene therapy.Frontiers in aging · 2026Article
- Telomerase mRNA-Lipid nanoparticles attenuate neuroinflammation after traumatic brain injury in mice.bioRxiv : the preprint server for biology · 2025Article
- Deletion of METTL14, a key methylation regulator, attenuates vascular ageing.European heart journal · 2025Article
- Article
- The dual guardians of cellular stability: exploring nesprin and lamin in senescence.Cell death & disease · 2025Review
- The Mechanism and Potential Therapeutic Strategies of Vascular Aging.Aging medicine (Milton (N.S.W)) · 2025Review
- Impact of miR-181a on SIRT1 Expression and Senescence in Hutchinson-Gilford Progeria Syndrome.Diseases (Basel, Switzerland) · 2025Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
aimsHutchinson-Gilford progeria syndrome (HGPS) is an accelerated ageing syndrome associated with premature vascular disease and death due to heart attack and stroke. In HGPS a mutation in lamin A (progerin) alters nuclear morphology and gene expression. Current therapy increases the lifespan of these children only modestly. Thus, greater understanding of the underlying mechanisms of HGPS is required to improve therapy. Endothelial cells (ECs) differentiated from induced pluripotent stem cells (iPSCs) derived from these patients exhibit hallmarks of senescence including replication arrest, increased expression of inflammatory markers, DNA damage, and telomere erosion. We hypothesized that correction of shortened telomeres may reverse these measures of vascular ageing. METHODS AND
resultsWe generated ECs from iPSCs belonging to children with HGPS and their unaffected parents. Telomerase mRNA (hTERT) was used to treat HGPS ECs. Endothelial morphology and functions were assessed, as well as proteomic and transcriptional profiles with attention to inflammatory markers, DNA damage, and EC identity genes. In a mouse model of HGPS, we assessed the effects of lentiviral transfection of mTERT on measures of senescence, focusing on the EC phenotype in various organs. hTERT treatment of human HGPS ECs improved replicative capacity; restored endothelial functions such as nitric oxide generation, acetylated low-density lipoprotein uptake and angiogenesis; and reduced the elaboration of inflammatory cytokines. In addition, hTERT treatment improved cellular and nuclear morphology, in association with a normalization of the transcriptional profile, effects that may be mediated in part by a reduction in progerin expression and an increase in sirtuin 1 (SIRT1). Progeria mice treated with mTERT lentivirus manifested similar improvements, with a reduction in inflammatory and DNA damage markers and increased SIRT1 in their vasculature and other organs. Furthermore, mTERT therapy increased the lifespan of HGPS mice.
conclusionVascular rejuvenation using telomerase mRNA is a promising approach for progeria and other age-related diseases.
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