ReviewAnnual review of pathology2022
Molecular Pathology of Laminopathies.
Review in Annual review of pathology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
76 citing papers in PubMed, 112 citations in OpenAlex.
- Nuclear mechanobiology rules immune cells' functions: from differentiation to cell trafficking and pathogen killing.Nucleus (Austin, Tex.) · 2026Review
- The responsive nucleus: morphological signatures of cellular state.Nucleus (Austin, Tex.) · 2026Review
- The risk of nephrotic range proteinuria and kidney failure in primary laminopathies is genotype specific.JCI insight · 2026Article
- Cardiomyocyte vulnerability to lamin polymer disruption revealed by saturation mutagenesis.bioRxiv : the preprint server for biology · 2026Article
- Article
- Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Progerin-induced nuclear envelope remodeling is shaped by cell division and NUP153.Journal of cell science · 2026Article
- Review
- Dysregulated nuclear Lamin B1 in DYT1 dystonia thickens nuclear lamina and disrupts 14-3-3 proteins.Cell death discovery · 2026Article
- A manually curated gene-phenotype catalogue for progeroid syndromes and premature aging.Aging · 2026Article
- CRISPR-mediated targeting of theMolecular therapy. Advances · 2026Article
- UBC9-mediated regulation of K144 ubiquitination of Lamin A and its implications for hepatocellular carcinoma.Journal of translational medicine · 2026Article
- LEM-Domain-Containing Inner Nuclear Membrane Proteins: Emerging Regulators of Intranuclear Signaling.International journal of molecular sciences · 2026Review
- Stress transmission towards the nucleus of the cell.Frontiers in cell and developmental biology · 2026Review
- Sterile inflammation in laminopathies.European journal of cell biology · 2025Review
- Immunosenescence in aging and neurodegenerative diseases: evidence, key hallmarks, and therapeutic implications.Translational neurodegeneration · 2025Review
- Mitotic dynamics of the nuclear lamina in the backstage of chromosome separation.Communications biology · 2025Review
- LMNA-related cardiomyopathy: From molecular pathology to cardiac gene therapy.Journal of advanced research · 2025Review
- Precise gene editing of pathogenic Lamin A mutations corrects cardiac disease.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Clinical Reasoning: A 63-Year-Old Female Patient Presenting With Orthostatic Hypotension and Ataxia.Neurology · 2025Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The nuclear envelope is composed of the nuclear membranes, nuclear lamina, and nuclear pore complexes. Laminopathies are diseases caused by mutations in genes encoding protein components of the lamina and these other nuclear envelope substructures. Mutations in the single gene encoding lamin A and C, which are expressed in most differentiated somatic cells, cause diseases affecting striated muscle, adipose tissue, peripheral nerve, and multiple systems with features of accelerated aging. Mutations in genes encoding other nuclear envelope proteins also cause an array of diseases that selectively affect different tissues or organs. In some instances, the molecular and cellular consequences of laminopathy-causing mutations are known. However, even when these are understood, mechanisms explaining specific tissue or organ pathology remain enigmatic. Current mechanistic hypotheses focus on how alterations in the nuclear envelope may affect gene expression, including via the regulation of signaling pathways, or cellular mechanics, including responses to mechanical stress.
Indexed as
Identifiers
What OpenQuestion holds
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.