ArticleAging cell2018
Increasing autophagy and blocking Nrf2 suppress laminopathy-induced age-dependent cardiac dysfunction and shortened lifespan.
Article in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 54 citations in OpenAlex.
- An Unbiased Drug Screen in a Drosophila Model ofInternational journal of molecular sciences · 2026Article
- Functional characterisation of rare variants in genes encoding the MAPK/ERK signalling pathway identified in long-lived Leiden Longevity Study participants.GeroScience · 2026Article
- Perinuclear organelle trauma at the nexus of cardiomyopathy pathogenesis arising from loss of functionNucleus (Austin, Tex.) · 2025Review
- Review
- Lamin variants cause cardiac arrhythmogenicity in Drosophila.Disease models & mechanisms · 2025Article
- Identifying links between cardiovascular disease and insomnia by modeling genes from a pleiotropic locus.Disease models & mechanisms · 2025Article
- A genetic variant inScience advances · 2025Article
- Novel And Efficient Method for Drosophila Heart Fluorescence Staining with Cryosectioning.Journal of visualized experiments : JoVE · 2025Article
- Model organisms for investigating the functional involvement of NRF2 in non-communicable diseases.Redox biology · 2025Review
- Molecular mechanism on autophagy associated cardiovascular dysfunction inFrontiers in cell and developmental biology · 2025Review
- Editorial: The role of autophagy in cardiovascular disease.Frontiers in cell and developmental biology · 2025Article
- Regulatory mechanisms of mAmerican journal of translational research · 2025Review
- A comprehensive analysis of the defense responses of Odontotermes formosanus (Shiraki) provides insights into the changes during Serratia marcescens infection.BMC genomics · 2024Article
- Review
- Automated assessment of cardiac dynamics in aging and dilated cardiomyopathy Drosophila models using machine learning.Communications biology · 2024Article
- From gene to mechanics: a comprehensive insight into the mechanobiology of LMNA mutations in cardiomyopathy.Cell communication and signaling : CCS · 2024Review
- The role of autophagy in the progression of HIV infected cardiomyopathy.Frontiers in cell and developmental biology · 2024Review
- Drosophila Models Reveal Properties of Mutant Lamins That Give Rise to Distinct Diseases.Cells · 2023Article
- The bridge between cell survival and cell death: reactive oxygen species-mediated cellular stress.EXCLI journal · 2023Review
- Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in the human LMNA gene cause a collection of diseases known as laminopathies. These include myocardial diseases that exhibit age-dependent penetrance of dysrhythmias and heart failure. The LMNA gene encodes A-type lamins, intermediate filaments that support nuclear structure and organize the genome. Mechanisms by which mutant lamins cause age-dependent heart defects are not well understood. To address this issue, we modeled human disease-causing mutations in the Drosophila melanogaster Lamin C gene and expressed mutant Lamin C exclusively in the heart. This resulted in progressive cardiac dysfunction, loss of adipose tissue homeostasis, and a shortened adult lifespan. Within cardiac cells, mutant Lamin C aggregated in the cytoplasm, the CncC(Nrf2)/Keap1 redox sensing pathway was activated, mitochondria exhibited abnormal morphology, and the autophagy cargo receptor Ref2(P)/p62 was upregulated. Genetic analyses demonstrated that simultaneous over-expression of the autophagy kinase Atg1 gene and an RNAi against CncC eliminated the cytoplasmic protein aggregates, restored cardiac function, and lengthened lifespan. These data suggest that simultaneously increasing rates of autophagy and blocking the Nrf2/Keap1 pathway are a potential therapeutic strategy for cardiac laminopathies.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.