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Article

Attenuated hypertrophic response to pressure overload in a lamin A/C haploinsufficiency mouse.

Journal of molecular and cellular cardiology - 1 Jun 2010

Cupesi Mihaela, Yoshioka Jun, Gannon Joseph, Kudinova Anastacia, Stewart Colin L, Lammerding Jan

Abstract excerpt

Inherited mutations cause approximately 30% of all dilated cardiomyopathy cases, with autosomal dominant mutations in the LMNA gene accounting for more than one third of these. The LMNA gene encodes the nuclear envelope proteins lamins A and C, which provide structural support to the nucleus and...

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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 19913544
DOI: 10.1016/j.yjmcc.2009.10.024
PMCID: PMC2866774

Genes

LMNA

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026. Prepared record publication-19913544-2026-09-02.2. Manifest publication-graph-cohort-2026-09-02.2.

Source receipt: PubMed via Helena Literature Corpus, retrieved 2 Sept 2026.

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Attenuated hypertrophic response to pressure overload in a lamin A/C haploinsufficiency mouse.PMID 19913544Read ↗

Effects of mechanical stress and carvedilol in lamin A/C-deficient dilated cardiomyopathy.Semantic proximity Read ↗

Lamin A/C Cardiomyopathy: Implications for Treatment.Semantic proximity Read ↗

Current insights into LMNA cardiomyopathies: Existing models and missing LINCs.Semantic proximity Read ↗

Age-dependent Lamin remodeling induces cardiac dysfunction via dysregulation of cardiac transcriptional programsSemantic proximity Read ↗

Perinuclear damage from nuclear envelope deterioration elicits stress responses that contribute to <i>LMNA</i> cardiomyopathySemantic proximity Read ↗

LMNA cardiomyopathy: cell biology and genetics meet clinical medicineSemantic proximity Read ↗

The Pathogenic Mechanisms of and Novel Therapies for Lamin A/C-Related Dilated Cardiomyopathy Based on Patient-Specific Pluripotent Stem Cell Platforms and Animal ModelsSemantic proximity Read ↗

Lamin A/C Ablation in Vascular Smooth Muscle Cells, Cardiomyocytes, and Cardiac Fibroblasts Causes Cardiac and Vascular Dysfunction: Role in the Pathophysiology of LMNA-Related Dilated CardiomyopathiesSemantic proximity Read ↗

Cardiomyocyte-specific expression of lamin a improves cardiac function in Lmna-/- mice.Semantic proximity Read ↗

Lamin A/C Ablation Restricted to Vascular Smooth Muscle Cells, Cardiomyocytes, and Cardiac Fibroblasts Causes Cardiac and Vascular Dysfunction.Semantic proximity Read ↗

Mitogen-activated protein kinase inhibitor regulation of heart function and fibrosis in cardiomyopathy caused by lamin A/C gene mutation.Semantic proximity Read ↗

Targeting Mitogen-Activated Protein Kinase Signaling in Mouse Models of Cardiomyopathy Caused by Lamin A/C Gene Mutations.Semantic proximity Read ↗

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