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Proteomics reveals mitochondrial dysfunction in Lmna-/- mice hearts

ABSTRACT: We performed proteomics analysis on Lmna-/- hearts from mice at 2 weeks and 1 month of age to investigate the underlying mechanism by which LMNA deletion evokes DCM

ORGANISM(S): Mus Musculus

SUBMITTER: Tong Yin

PROVIDER: PXD043270 | iProX | Sun Jun 25 00:00:00 BST 2023

REPOSITORIES: iProX

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SIRT1 Ameliorates Lamin A/C Deficiency-Induced Cardiac Dysfunction by Promoting Mitochondrial Bioenergetics.

Du Zunhui Z Zhou Yanting Y Li Qiheng Q Xie Yuan Y Zhu Tingfang T Qiao Jing J Zhang Ruihong R Bao Yangyang Y Wang Lingjie L Xie Yinyin Y Quan Jinwei J Lin Menglu M Zhang Ning N Jin Qi Q Liang Wenbin W Wu Liqun L Yin Tong T Xie Yucai Y

JACC. Basic to translational science 20240731 10

Dilated cardiomyopathy (DCM) is associated with high mortality despite advanced therapies. The LMNA gene encodes lamin A/C and is the second most frequently mutated gene associated with DCM, for which therapeutic options are limited. Here we generated Lmna -/- mice and found they exhibited cardiac dysfunction at the age of 1 month but not at 2 weeks. Proteomics showed down-regulation of mitochondrial function-related pathways in Lmna -/- hearts. Moreove ...[more]

PMID: 39534638

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