Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Temsirolimus activates autophagy and ameliorates cardiomyopathy caused by lamin A/C gene mutation.

Science translational medicine - 25 Jul 2012

Choi Jason C, Muchir Antoine, Wu Wei, Iwata Shinichi, Homma Shunichi, Morrow John P, Worman Howard J

Abstract excerpt

Mutations in the lamin A/C gene (LMNA), which encodes A-type lamins, cause a diverse range of diseases collectively called laminopathies, the most common of which is dilated cardiomyopathy. Emerging evidence suggests that LMNA mutations cause disease by altering cell signaling pathways, but the specific mechanisms are poorly understood. We show that the AKT-mammalian target of rapamycin pathway is hyperactivated...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Autophagy
Share to Cardiomyopathies

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to LMNA gene

Share to Lamin Type A

Share to Mutation

Share to Sirolimus

Source

Open in PubMed Open full text

Identifiers

PMID: 22837537
DOI: 10.1126/scitranslmed.3003875
PMCID: PMC3700376

Genes

LMNA

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Temsirolimus activates autophagy and ameliorates cardiomyopathy caused by lamin A/C gene mutation.PMID 22837537Read ↗

mTOR Inhibition Prolongs Survival and Has Beneficial Effects on Heart Function After Onset of Lamin A/C Gene Mutation Cardiomyopathy in Mice.Semantic proximity Read ↗

Cell signaling abnormalities in cardiomyopathy caused by lamin A/C gene mutations.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 ↗

AZD2014, A Dual mTOR Inhibitor, Attenuates Cardiac Hypertrophy in Vitro and in VivoSemantic proximity Read ↗

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

mTOR Hyperactivation by Ablation of Tuberous Sclerosis Complex 2 in the Mouse Heart Induces Cardiac Dysfunction with the Increased Number of Small Mitochondria Mediated through the Down-Regulation of Autophagy.Semantic proximity Read ↗

The roles of the inhibitory autophagy regulator Rubicon in the heart: A new therapeutic target to prevent cardiac cell deathSemantic proximity Read ↗

Activation of Autophagy Ameliorates Cardiomyopathy in Mybpc3-Targeted Knockin Mice.Semantic proximity Read ↗

Autophagy activation can partially rescue proteasome dysfunction‐mediated cardiac toxicitySemantic proximity Read ↗

Treatment with selumetinib preserves cardiac function and improves survival in cardiomyopathy caused by mutation in the lamin A/C gene.Semantic proximity Read ↗

Rapamycin reverses hypertrophic cardiomyopathy in a mouse model of LEOPARD syndrome-associated PTPN11 mutation.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.