ArticlePloS one2010
LMNA E82K mutation activates FAS and mitochondrial pathways of apoptosis in heart tissue specific transgenic mice.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Correlation of Long Non-Coding RNAs and Gene Expression in Response to Reverse Development of Turritopsis dohrnii.Marine biotechnology (New York, N.Y.) · 2026Article
- Review
- Attenuated lamin A-prohibitin2 interaction leads to mitochondrial dysfunction in LMNA 289 A>G-mediated dilated cardiomyopathy.The Journal of biological chemistry · 2026Article
- Metabolic Dysregulation in Laminopathies: Implications for Heart Failure and Cardiac Health.Current heart failure reports · 2026Review
- Perinuclear organelle trauma at the nexus of cardiomyopathy pathogenesis arising from loss of functionNucleus (Austin, Tex.) · 2025Review
- LMNA-related cardiomyopathy: From molecular pathology to cardiac gene therapy.Journal of advanced research · 2025Review
- Cardiac phenotypes in LMNA mutations.Current opinion in cardiology · 2025Review
- The Pathogenic Mechanisms of and Novel Therapies for Lamin A/C-Related Dilated Cardiomyopathy Based on Patient-Specific Pluripotent Stem Cell Platforms and Animal Models.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Global Proteomic Analysis Reveals Alterations in Differentially Expressed Proteins between Cardiopathic Lamin A/C Mutations.Journal of proteome research · 2024Article
- Perinuclear damage from nuclear envelope deterioration elicits stress responses that contribute toScience advances · 2024Article
- Quantitative proteomic profiling identifies global protein network dynamics in murine embryonic heart development.Developmental cell · 2023Article
- Epigenetics inCells · 2023Review
- Novel rat model of multiple mitochondrial dysfunction syndromes (MMDS) complicated with cardiomyopathy.Animal models and experimental medicine · 2021Article
- Identification of Target Genes and Transcription Factors in Mice with LMNA-Related Dilated Cardiomyopathy by Integrated Bioinformatic Analyses.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Downregulation of Cypher induces apoptosis in cardiomyocytes via Akt/p38 MAPK signaling pathway.International journal of medical sciences · 2020Article
- Lamin A/C Cardiomyopathy: Implications for Treatment.Current cardiology reports · 2019Review
- Review
- Genetic mutation of familial dilated cardiomyopathy based on next‑generation semiconductor sequencing.Molecular medicine reports · 2018Article
- Cardiac ageing: extrinsic and intrinsic factors in cellular renewal and senescence.Nature reviews. Cardiology · 2018Review
- Linker of nucleoskeleton and cytoskeleton complex proteins in cardiomyopathy.Biophysical reviews · 2018Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lamin A/C (LMNA), nuclear intermediate filament proteins, is a basic component of the nuclear lamina. Mutations in LMNA are associated with a broad range of laminopathies, congenital diseases affecting tissue regeneration and homeostasis. Heart tissue specific transgenic mice of human LMNA E82K, a mutation causing dilated cardiomyopathy, were generated. Lmna(E82K) transgenic mouse lines exhibited thin-walled, dilated left and right ventricles, a progressive decrease of contractile function assessed by echocardiography. Abnormalities of the conduction system, myocytes disarray, collagen accumulation and increased levels of B-type natriuretic peptide (BNP), procollagen type III α1 (Col3α1) and skeletal muscle actin α1 (Actα1) were detected in the hearts of Lmna(E82K) transgenic mice. The LMNA E82K mutation caused mislocation of LMNA in the nucleus and swollen mitochondria with loss of critae, together with the loss of nuclear envelope integrity. Most interestingly, we found that the level of apoptosis was 8.5-fold higher in the Lmna(E82K) transgenic mice than that of non-transgenic (NTG) mice. In the presence of the LMNA E82K, both of FAS and mitochondrial pathways of apoptosis were activated consistent with the increase of FAS expression, the release of cytochrome c from mitochondria to cytosol and activation of caspase-8, -9 and -3. Our results suggested that the apoptosis, at least for the LMNA E82K or the mutations in the rod region of Lamin A/C, might be an important mechanism causing continuous loss of myocytes and lead to myocardial dysfunction. It could be a potential therapeutic means to suppress and/or prevent inappropriate cardiac cell death in patients carrying LMNA mutation.
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