Citation only
via Europe PMC
Biomarkers and therapies Associated with Hutchinson-Gilford Syndrome.
Ali RS, Cao Z, Zhou X, Wang G, He H, Du Z, Li Y, Chen L, Hu L.
Ageing research reviews · 2026
Genomic instability
Telomere attrition
Epigenetic alterations
Deregulated nutrient-sensing
Mitochondrial dysfunction
Cellular senescence
Altered intercellular communication
Chronic inflammation
Senolytics
Partial reprogramming (OSK)
Human
Mouse
Preclinical / animal
Abstract
Hutchinson-Gilford progeria syndrome (HGPS) is an ultra-rare premature aging disorder caused predominantly by a de novo LMNA c.1824C>T mutation that produces progerin, a truncated and permanently farnesylated lamin A isoform. Progerin accumulation disrupts nuclear lamina integrity and chromatin organization, inducing persistent DNA damage responses, telomere(definition) attrition, mitochondrial dysfunction(definition), and cellular senescence(definition). These processes drive a multisystem clinical phenotype characterized by growth impairment, lipodystrophy, musculoskeletal abnormalities, and rapidly progressive vascular disease, with cardiovascular events as the leading cause of mortality. Biomarkers could be used in clinical trails and preclinical models for research purposes. Current candidates span four major categories: (i) molecular markers, including LMNA genotype, progerin levels, γH2AX/pATM signaling, telomere shortening, and epigenetic alterations; (ii) cellular markers reflecting oxidative stress, mitochondrial impairment, and senescence-associated secretory phenotype (SASP); (iii) systemic inflammatory and immune mediators; and (iv) vascular structural and functional indices such as arterial stiffness and endothelial dysfunction, which correlate strongly with survival. Preclinical progeroid mouse models and LMNA-edited minipigs have facilitated translational validation of these biomarker axes. Therapeutic approaches now extend beyond farnesyltransferase inhibition. Lonafarnib improves vascular outcomes and survival; however, persistent cardiovascular decline indicates residual unmet need. Emerging interventions-including mTOR(definition) modulation, senolytics(definition), anti-inflammatory agents, metabolic support, antisense oligonucleotides, and gene-editing strategies targeting progerin production-may benefit from biomarker-guided implementation. The integration of multi-parameter biomarker panels with mechanism-based combination therapies represents a promising direction toward precision management in HGPS.
◌ CITATION ONLY
Full text is not openly licensed for redistribution here. Read it at the source:
Provenance
- Source
- Europe PMC
- DOI
- 10.1016/j.arr.2026.103209
- Canonical
- link ↗
- Fetched
- 2026-07-01 MST
Cite this
APA
RS, A., Z, C., X, Z., G, W., H, H., Z, D., Y, L., L, C., & L., H. (2026). Biomarkers and therapies Associated with Hutchinson-Gilford Syndrome. <em>Ageing research reviews</em>. https://doi.org/10.1016/j.arr.2026.103209
Vancouver
RS A, Z C, X Z, G W, H H, Z D, et al. Biomarkers and therapies Associated with Hutchinson-Gilford Syndrome. Ageing research reviews. 2026. doi:10.1016/j.arr.2026.103209.
BibTeX
@article{ali2026Biomar,
title = {Biomarkers and therapies Associated with Hutchinson-Gilford Syndrome.},
author = {Ali RS and Cao Z and Zhou X and Wang G and He H and Du Z and Li Y and Chen L and Hu L.},
journal = {Ageing research reviews},
year = {2026},
doi = {10.1016/j.arr.2026.103209},
}
Research neighborhood
References, citing works, and semantically nearest findings. Click a node to open it.
Related findings
Biology of sport 2026
Open access · OA
Aging reimagined: Bridging clinical modulation and scientific breakthroughs.
Biogerontology 2026
Citation only
Aging-modulatory effects of Pausinystalia macroceras (K. Schum.) Pierre polysaccharides are associated with DAF-16/FOXO and SKN-1/Nrf2 signaling in multiple aging models.
Biomolecules 2025
Open access · CC-BY
Proteostasis Decline and Redox Imbalance in Age-Related Diseases: The Therapeutic Potential of NRF2
Journal of Integrative Medicine and Research 2026
Open access · CC-BY
How old are you really? Epigenetic clocks – A narrative review
Biological Rhythm Research 2026
Citation only
Dynamic integration of metabolic, circadian and neuroendocrine axes in ageing and regeneration from the cellular and molecular perspectives
Geriatrics and gerontology international/Geriatrics & gerontology international 2016
Open access · OA