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Article

Lamin A/C deficiency-mediated ROS elevation contributes to pathogenic phenotypes of dilated cardiomyopathy in iPSC model.

Nature communications - 14 Aug 2024

Qiu Hangyuan, Sun Yaxun, Wang Xiaochen, Gong Tingyu, Su Jun, Shen Jiaxi, Zhou Jingjun, Xia Jiafeng, Wang Hao, Meng Xiangfu, Fu Guosheng, Zhang Donghui, Jiang Chenyang, Liang Ping

Abstract excerpt

Mutations in the nuclear envelope (NE) protein lamin A/C (encoded by LMNA), cause a severe form of dilated cardiomyopathy (DCM) with early-onset life-threatening arrhythmias. However, molecular mechanisms underlying increased arrhythmogenesis in LMNA-related DCM (LMNA-DCM) remain largely unknown. Here we show that a frameshift mutation in LMNA causes abnormal Ca2+ handling, arrhythmias and disformed NE in...

Read the complete abstract on PubMed

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Share to Arrhythmias, Cardiac
Share to Calcium-Calmodulin-Dependent Protein Kinase Type 2

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Cardiomyopathy, Dilated

Share to Lamin Type A

Share to Myocytes, Cardiac

Share to Nuclear Envelope

Share to Ryanodine Receptor Calcium Release Channel

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Source

Open in PubMed Open full text

Identifiers

PMID: 39143095
DOI: 10.1038/s41467-024-51318-5
PMCID: PMC11324749

Genes

LMNA
SIRT1
RYR2
SUN1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

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