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This report details two patients with Hutchinson-Gilford Progeria syndrome who exhibited generalized shiny skin in infancy and had a novel mutation in the LMNA gene.

In Arabidopsis thaliana, this study found that proper O-glycosylation of extensins is crucial for root hair elongation and self-assembly of the cell wall.

In this study, researchers identified novel LMNA mutations in patients with atypical progeroid syndrome, revealing clinical features distinct from other similar disorders, but unrelated to mutant prelamin A accumulation.

This review discusses the role of lamins in development, tissue maintenance, and stress response, and does not report new experimental findings.

This study found that intermittent treatment with FTI lonafarnib and sulforaphane may be a promising therapeutic approach for children with Hutchinson-Gilford progeria syndrome, as it improved the cellular phenotype.

This review explores how cell and mouse models have contributed to understanding the mechanisms of human aging, particularly focusing on Hutchinson-Gilford Progeria Syndrome, and reports no new clinical results.

This paper reviews the role of endoplasmic reticulum stress and the unfolded protein response in Hutchinson-Gilford progeria syndrome-related atherosclerosis, especially in vascular smooth muscle cells, but reports no clinical findings; intervention in these pathways is suggested as a potential therapeutic strategy.

In this study, baricitinib treatment improved the differentiation of skin-derived precursors into adipocytes for diseases like Hutchinson-Gilford progeria syndrome, suggesting potential benefits when combined with lonafarnib.

This review discusses Hutchinson-Gilford progeria syndrome, highlighting its phenotype, pathogenesis, and its potential insights into natural aging and cardiovascular diseases, but it reports no new research findings.

In this study, researchers found that correcting the HGPS mutation with Adenine base editing partially rescued accelerated skin cell differentiation and reduced cell death in patient-derived stem cells.

This article reviews treatments for progeria, including aspirin, hydrotherapy, and farnesyl transferase inhibitors, but reports no new clinical results.

This review discusses genetic mutations associated with Hutchinson-Gilford progeria syndrome and reports no clinical results; the authors emphasize the importance of cardiovascular monitoring in management.

This study found that in Hutchinson–Gilford progeria syndrome, iPSCs committed to the keratinocyte lineage faster than normal cells, with LEF1 expression reduced and a partial rescue of the phenotype achieved through adenine base editing.

This review discusses Hutchinson-Gilford Progeria Syndrome, its symptomatology, and the progress in developing treatment strategies, emphasizing that while a cure remains elusive, advances in understanding the disease's molecular mechanisms show promise for future approaches.

This case report from Nepal describes a five-year-old boy with Hutchinson Gilford Progeria Syndrome experiencing ocular manifestations, highlighting the role of ocular senescence in this genetic disorder.

This chapter reviews Hutchinson–Gilford progeria syndrome as a model for studying aging but presents no new findings, covering its genetic basis, clinical features, and existing treatments.

This study explored the effects of a common Hutchinson-Gilford progeria syndrome mutation in an inducible mouse model, revealing skin abnormalities similar to those in affected patients.

In this study, a transgenic mouse model suggested that suppressing the expression of the HGPS mutation may reverse disease symptoms, including skin abnormalities, supporting the potential for treatment development.

In this study, the researchers reported a new case of Hutchinson-Gilford progeria syndrome with a novel LMNA mutation and successful surgical intervention for airway obstruction.

This article reviews current understanding of Hutchinson–Gilford Progeria Syndrome and suggests RNA-based treatments show promise, but no new clinical findings are reported.

This review covers the history, symptoms, and treatment progress for Hutchinson-Gilford Progeria Syndrome, noting that while no cure exists, understanding its molecular mechanism may improve future treatment strategies.

This study found that although progerin expression in mouse skin causes significant nuclear shape changes in keratinocytes, it does not result in alopecia or common skin abnormalities seen in human Hutchinson–Gilford progeria syndrome.

This review discusses the molecular mechanisms of Hutchinson-Gilford progeria syndrome and evaluates current research trends, available mouse models, and prospects for developing therapies, but reports no new clinical findings.

This study reported that inhibiting the JAK-STAT pathway with baricitinib restored cellular homeostasis, delayed senescence, and reduced proinflammatory markers in Hutchinson-Gilford progeria syndrome cell models.

This study suggests that disruptions in the Ran system related to nuclear transport may be a key factor in the development of cellular issues in Hutchinson Gilford Progeria Syndrome.

This study created transgenic mouse models with the LMNA gene mutation common in Hutchinson-Gilford progeria syndrome, revealing skin and teeth abnormalities related to transgene expression levels.

This case report details the ocular complications of Hutchinson-Gilford Progeria syndrome in a 20-year-old Bangladeshi patient, highlighting symptoms like dry eyes, Meibomian gland dysfunction, and cataracts.

This review discusses how the nuclear lamina integrates biochemical and mechanical signals to influence gene expression and skin homeostasis, but reports no new clinical results.

This study found that restoring hypothalamic NPY levels in mice delayed aging-related characteristics such as fat loss, hair loss, and memory decline, suggesting that maintaining these levels could be important for counteracting aging and its effects.

This review discusses the molecular pathology of progeroid syndromes and reports no new results; the authors emphasize understanding these mechanisms to develop treatments and potentially improve quality of life for affected individuals.