ReviewFrontiers in cell and developmental biology2018
Induced Pluripotent Stem Cells to Study Mechanisms of Laminopathies: Focus on Epigenetics.
Review in Frontiers in cell and developmental biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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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
9 citing papers in PubMed, 19 citations in OpenAlex.
- Selection of specific and efficient siRNAs in new cellular model for Hutchinson-Gilford progeria syndrome therapy.Molecular therapy. Nucleic acids · 2025Article
- Clinical and metabolic consequences of a historic pathogenic lamin A/C founder variant.Scientific reports · 2025Article
- Human iPSC-Derived Muscle Cells as a New Model for Investigation of EDMD1 Pathogenesis.International journal of molecular sciences · 2025Article
- Inflammation and Fibrosis in Progeria: Organ-Specific Responses in an HGPS Mouse Model.International journal of molecular sciences · 2024Article
- Article
- Article
- Effect of Occurrence of Lamin A/C (Frontiers in cardiovascular medicine · 2022Article
- Most myopathic lamin variants aggregate: a functional genomics approach for assessing variants of uncertain significance.NPJ genomic medicine · 2021Article
- Diversity of Nuclear Lamin A/C Action as a Key to Tissue-Specific Regulation of Cellular Identity in Health and Disease.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Laminopathies are a group of rare degenerative disorders that manifest with a wide spectrum of clinical phenotypes, including both systemic multi-organ disorders, such as the Hutchinson-Gilford Progeria Syndrome (HGPS), and tissue-restricted diseases, such as Emery-Dreifuss muscular dystrophy, dilated cardiomyopathy and lipodystrophies, often overlapping. Despite their clinical heterogeneity, which remains an open question, laminopathies are commonly caused by mutations in the LMNA gene, encoding the nuclear proteins Lamin A and C. These two proteins are main components of the nuclear lamina and are involved in several biological processes. Besides the well-known structural function in the nucleus, their role in regulating chromatin organization and transcription has emerged in the last decade, supporting the hypothesis that the disruption of this layer of regulation may be mechanism underlying the disease. Indeed, recent studies that show various epigenetic defects in cells carrying LMNA mutations, such as loss of heterochromatin, changes in gene expression and chromatin remodeling, strongly support this view. However, those findings are restricted to few cell types in humans, mainly because of the limited accessibility of primary cells and the difficulties to culture them
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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.