ArticleJCI insight2019
Prelamin A mediates myocardial inflammation in dilated and HIV-associated cardiomyopathies.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 46 citations in OpenAlex.
- Lamin B1 loss in human cardiomyocytes is associated with nuclear shape deformation in dilated cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026Article
- Sterile inflammation in laminopathies.European journal of cell biology · 2025Review
- LMNA-related cardiomyopathy: From molecular pathology to cardiac gene therapy.Journal of advanced research · 2025Review
- Mineral Stress Drives Loss of Heterochromatin: An Early Harbinger of Vascular Inflammaging and Calcification.Circulation research · 2025Article
- Ischemic cardiac stromal fibroblast-derived protein mediators in the infarcted myocardium and transcriptomic profiling at single cell resolution.Functional & integrative genomics · 2024Article
- Mechanical overloading leads to chondrocyte degeneration and senescence via Zmpste24-mediated nuclear membrane instability.iScience · 2023Article
- Myocardial Inflammation as a Manifestation of Genetic Cardiomyopathies: From Bedside to the Bench.Biomolecules · 2023Review
- Review
- Lamin A precursor localizes to the Z-disc of sarcomeres in the heart and is dynamically regulated in muscle cell differentiation.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022Article
- Human Immunodeficiency Virus Infection-Associated Cardiomyopathy and Heart Failure.Journal of personalized medicine · 2022Review
- Bioinformatics prediction of potential mechanisms and biomarkers underlying dilated cardiomyopathy.World journal of cardiology · 2022Article
- Antiretroviral Therapy-Induced Dysregulation of Gene Expression and Lipid Metabolism in HIV+ Patients: Beneficial Role of Antioxidant Phytochemicals.International journal of molecular sciences · 2022Review
- Abolishing the prelamin A ZMPSTE24 cleavage site leads to progeroid phenotypes with near-normal longevity in mice.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Identification and Verification of Feature Biomarkers Associated With Immune Cells in Dilated Cardiomyopathy by Bioinformatics Analysis.Frontiers in genetics · 2022Article
- Etiology and pathophysiology of heart failure in people with HIV.Heart failure reviews · 2021Review
- Intermediate filaments as effectors of differentiation.Current opinion in cell biology · 2021Review
- Metformin inhibits chronic kidney disease-induced DNA damage and senescence of mesenchymal stem cells.Aging cell · 2021Article
- Distinct Myocardial Transcriptomic Profiles of Cardiomyopathies Stratified by the Mutant Genes.Genes · 2020Article
- Article
- Using nuclear envelope mutations to explore age-related skeletal muscle weakness.Clinical science (London, England : 1979) · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Cardiomyopathies are complex heart muscle diseases that can be inherited or acquired. Dilated cardiomyopathy can result from mutations in LMNA, encoding the nuclear intermediate filament proteins lamin A/C. Some LMNA mutations lead to accumulation of the lamin A precursor, prelamin A, which is disease causing in a number of tissues, yet its impact upon the heart is unknown. Here, we discovered myocardial prelamin A accumulation occurred in a case of dilated cardiomyopathy, and we show that a potentially novel mouse model of cardiac-specific prelamin A accumulation exhibited a phenotype consistent with inflammatory cardiomyopathy, which we observed to be similar to HIV-associated cardiomyopathy, an acquired disease state. Numerous HIV protease therapies are known to inhibit ZMPSTE24, the enzyme responsible for prelamin A processing, and we confirmed that accumulation of prelamin A occurred in HIV+ patient cardiac biopsies. These findings (a) confirm a unifying pathological role for prelamin A common to genetic and acquired cardiomyopathies; (b) have implications for the management of HIV patients with cardiac disease, suggesting protease inhibitors should be replaced with alternative therapies (i.e., nonnucleoside reverse transcriptase inhibitors); and (c) suggest that targeting inflammation may be a useful treatment strategy for certain forms of inherited cardiomyopathy.
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.