ArticleProceedings of the National Academy of Sciences of the United States of America2017
HSPB7 is indispensable for heart development by modulating actin filament assembly.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 3 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 3 syntheses or guidelines pooled it, 86 citations in OpenAlex.
- Genome-wide association study meta-analysis provides insights into the etiology of heart failure and its subtypes.Nature genetics · 2025Pooled it
- Meta-analysis of genome-wide associations and polygenic risk prediction for atrial fibrillation in more than 180,000 cases.Nature genetics · 2025Pooled it
- Shared genetic pathways contribute to risk of hypertrophic and dilated cardiomyopathies with opposite directions of effect.Nature genetics · 2021Pooled it
- Kernelized approach enables explainable gene prioritizations for complex traits.bioRxiv : the preprint server for biology · 2026Article
- Sphingosine-1-phosphate receptor 1 signaling stimulates human pluripotent stem cell-derived cardiomyocyte differentiation and maturation.Experimental & molecular medicine · 2026Article
- Article
- 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
- Novel leiomodin 2b crispant zebrafish as a model for dilated cardiomyopathy.microPublication biology · 2026Article
- The Utility of Genome-Wide Association Studies in Inherited Arrhythmias and Cardiomyopathies.Genes · 2025Review
- Proteomic Analysis of Thin Filament Components Elucidates Changes in Spastic Muscle Sarcomere After Stroke.International journal of molecular sciences · 2025Article
- RBPMS and RBPMS2 Cooperate to Safeguard Cardiac Splicing.Circulation research · 2025Article
- Filamin C dimerisation is regulated by HSPB7.Nature communications · 2025Article
- Genome-wide association study reveals mechanisms underlying dilated cardiomyopathy and myocardial resilience.Nature genetics · 2024Article
- Heat shock protein B7 (HSPB7) inhibits lung adenocarcinoma progression by inhibiting glycolysis.Oncology reports · 2023Article
- Review
- HSPB7 oppositely regulates human mesenchymal stromal cell-derived osteogenesis and adipogenesis.Stem cell research & therapy · 2023Article
- HIV, asymptomatic STI, and the rectal mucosal immune environment among young men who have sex with men.PLoS pathogens · 2023Article
- Heat Shock Proteins: Important Helpers for the Development, Maintenance and Regeneration of Skeletal Muscles.Muscles (Basel, Switzerland) · 2023Review
- Efficacy of electroacupunture at Zusanli (ST36) on jumping-injured muscle based on transcriptome sequencing and genes analysis.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2023Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Small heat shock protein HSPB7 is highly expressed in the heart. Several mutations within HSPB7 are associated with dilated cardiomyopathy and heart failure in human patients. However, the precise role of HSPB7 in the heart is still unclear. In this study, we generated global as well as cardiac-specific HSPB7 KO mouse models and found that loss of HSPB7 globally or specifically in cardiomyocytes resulted in embryonic lethality before embryonic day 12.5. Using biochemical and cell culture assays, we identified HSPB7 as an actin filament length regulator that repressed actin polymerization by binding to monomeric actin. Consistent with HSPB7's inhibitory effects on actin polymerization, HSPB7 KO mice had longer actin/thin filaments and developed abnormal actin filament bundles within sarcomeres that interconnected Z lines and were cross-linked by α-actinin. In addition, loss of HSPB7 resulted in up-regulation of Lmod2 expression and mislocalization of Tmod1. Furthermore, crossing HSPB7 null mice into an Lmod2 null background rescued the elongated thin filament phenotype of HSPB7 KOs, but double KO mice still exhibited formation of abnormal actin bundles and early embryonic lethality. These in vivo findings indicated that abnormal actin bundles, not elongated thin filament length, were the cause of embryonic lethality in HSPB7 KOs. Our findings showed an unsuspected and critical role for a specific small heat shock protein in directly modulating actin thin filament length in cardiac muscle by binding monomeric actin and limiting its availability for polymerization.
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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.