ArticlePLoS genetics2017
HSPB7 prevents cardiac conduction system defect through maintaining intercalated disc integrity.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 44 citations in OpenAlex.
- Senescence dynamics define therapeutic windows for Duchenne muscular dystrophy in DBA/2-mdx mice.Skeletal muscle · 2026Article
- Genomic structural equation modeling reveals shared genetic structure of cardiac function and structure-function association studies of CLCNKA mutations.Scientific reports · 2026Article
- Effect of Mutations in the C-Terminal 22-24 Domains of Filamin C Associated with Cardio- and Myopathies on Its Interaction with Small Heat Shock Protein HspB7.International journal of molecular sciences · 2025Article
- Filamin C dimerisation is regulated by HSPB7.Nature communications · 2025Article
- Small HSPs at the crossroad between protein aggregation, autophagy and unconventional secretion: clinical implications and potential therapeutic opportunities in the context of neurodegenerative diseases.Frontiers in cell and developmental biology · 2025Review
- Reduction of Filamin C Results in Altered Proteostasis, Cardiomyopathy, and Arrhythmias.Journal of the American Heart Association · 2024Article
- Exploring the origins of neurodevelopmental proteasomopathies associated with cardiac malformations: are neural crest cells central to certain pathological mechanisms?Frontiers in cell and developmental biology · 2024Article
- Review
- HSPB7 oppositely regulates human mesenchymal stromal cell-derived osteogenesis and adipogenesis.Stem cell research & therapy · 2023Article
- The Role of Small Heat Shock Proteins in Protein Misfolding Associated Motoneuron Diseases.International journal of molecular sciences · 2022Review
- Insights on Human Small Heat Shock Proteins and Their Alterations in Diseases.Frontiers in molecular biosciences · 2022Review
- A Combined HumanFrontiers in pharmacology · 2022Article
- Linking metabolic dysfunction with cardiovascular diseases: Brn-3b/POU4F2 transcription factor in cardiometabolic tissues in health and disease.Cell death & disease · 2021Review
- HSPB7 regulates osteogenic differentiation of human adipose derived stem cells via ERK signaling pathway.Stem cell research & therapy · 2020Article
- Small heat-shock proteins and their role in mechanical stress.Cell stress & chaperones · 2020Review
- Mechanisms of Small Heat Shock Proteins.Cold Spring Harbor perspectives in biology · 2019Review
- Role of Bcl2-associated Athanogene 3 in Turnover of Gap Junction Protein, Connexin 43, in Neonatal Cardiomyocytes.Scientific reports · 2019Article
- Review
- HSPB7 is indispensable for heart development by modulating actin filament assembly.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HSPB7 is a member of the small heat-shock protein (HSPB) family and is expressed in the cardiomyocytes from cardiogenesis onwards. A dramatic increase in HSPB7 is detected in the heart and blood plasma immediately after myocardial infarction. Additionally, several single-nucleotide polymorphisms of HSPB7 have been identified to be associated with heart failure caused by cardiomyopathy in human patients. Although a recent study has shown that HSPB7 is required for maintaining myofiber structure in skeletal muscle, its molecular and physiological functions in the heart remain unclear. In the present study, we generated a cardiac-specific inducible HSPB7 knockout mouse and demonstrated that the loss of HSPB7 in cardiomyocytes results in rapid heart failure and sudden death. The electrocardiogram showed cardiac arrhythmia with abnormal conduction in the HSPB7 mutant mice before death. In HSPB7 CKO cardiomyocytes, no significant defect was detected in the organization of contractile proteins in sarcomeres, but a severe structural disruption was observed in the intercalated discs. The expression of connexin 43, a gap-junction protein located at the intercalated discs, was downregulated in HSPB7 knockout cardiomyocytes. Mislocalization of desmoplakin, and N-cadherin, the intercalated disc proteins, was also observed in the HSPB7 CKO hearts. Furthermore, filamin C, the interaction protein of HSPB7, was upregulated and aggregated in HSPB7 mutant cardiomyocytes. In conclusion, our findings characterize HSPB7 as an intercalated disc protein and suggest it has an essential role in maintaining intercalated disc integrity and conduction function in the adult heart.
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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.