ArticleCardiovascular research2019
Cardiomyocyte-specific deficiency of HSPB1 worsens cardiac dysfunction by activating NFκB-mediated leucocyte recruitment after myocardial infarction.
Article in Cardiovascular research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 65 citations in OpenAlex.
- Cardiomyocyte-derived HSPB1 regulates TGF-β1 maturation and inhibits endothelial-to-mesenchymal transition in myocardial fibrosis.iScience · 2026Article
- Pharmacological Inhibition of the HSPB1-NF-κB Axis Alleviates Brain Injury in a Rat Veno-Venous Extracorporeal Membrane Oxygenation Model.Molecular neurobiology · 2026Article
- Downregulation of HSPB1 and MGST1 Promotes Ferroptosis and Impacts Immune Infiltration in Diabetic Cardiomyopathy.Cardiovascular toxicology · 2025Article
- PLL-g-HPA Hydrogel Loaded Human Umbilical Cord Mesenchymal Stem Cells Promote Burn Wound Healing in Rat Model by Regulating Inflammation Response.Journal of inflammation research · 2025Article
- HSPA12A acts as a scaffolding protein to inhibit cardiac fibroblast activation and cardiac fibrosis.Journal of advanced research · 2025Article
- KMV-mediated cardiomyocyte-to-endothelial cell signaling drives capillary rarefaction to promote heart failure following pressure overload.Theranostics · 2025Article
- Humanin reduces nucleus pulposus cells ferroptosis to alleviate intervertebral disc degeneration: An in vitro and in vivo study.Journal of orthopaedic translation · 2025Article
- Mechanisms and Therapeutic Strategies for Myocardial Ischemia-Reperfusion Injury in Diabetic States.ACS pharmacology & translational science · 2024Review
- Down-regulation of HSPB1 and MGST1 promote ferroptosis and impact immune infiltration in diabetic cardiomyopathy.Research square · 2024Article
- HSPA12A maintains aerobic glycolytic homeostasis and Histone3 lactylation in cardiomyocytes to attenuate myocardial ischemia/reperfusion injury.JCI insight · 2024Article
- Proteomic analysis of plasma proteins from patients with cardiac rupture after acute myocardial infarction using TMT-based quantitative proteomics approach.Clinical proteomics · 2024Article
- Cardiac-specific deletion of BRG1 ameliorates ventricular arrhythmia in mice with myocardial infarction.Acta pharmacologica Sinica · 2024Article
- Article
- Brg1 and RUNX1 synergy in regulating TRPM4 channel in mouse cardiomyocytes.Frontiers in pharmacology · 2024Article
- Mapping the cellular and molecular landscape of cardiac non-myocytes in murine diabetic cardiomyopathy.iScience · 2023Article
- Insights gained from single-cell RNA analysis of murine endothelial cells in aging hearts.Heliyon · 2023Article
- The traditional Chinese medicines treat chronic heart failure and their main bioactive constituents and mechanisms.Acta pharmaceutica Sinica. B · 2023Review
- Mechanistic insights into heat shock protein 27, a potential therapeutic target for cardiovascular diseases.Frontiers in cardiovascular medicine · 2023Review
- Targeting WWP1 ameliorates cardiac ischemic injury by suppressing KLF15-ubiquitination mediated myocardial inflammation.Theranostics · 2023Article
- Risk prediction model construction for post myocardial infarction heart failure by blood immune B cells.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
Abstract
Aims: Inadequate healing after myocardial infarction (MI) leads to heart failure and fatal ventricular rupture, while optimal healing requires timely induction and resolution of inflammation. This study tested the hypothesis that heat shock protein B1 (HSPB1), which limits myocardial inflammation during endotoxemia, modulates wound healing after MI. Methods and results: To test this hypothesis, cardiomyocyte-specific HSPB1 knockout (Hspb1-/-) mice were generated using the Cre-LoxP recombination system. MI was induced by ligation of the left anterior descending coronary artery in Hspb1-/- and wild-type (WT) littermates. HSPB1 was up-regulated in cardiomyocytes of WT animals in response to MI, and deficiency of cardiomyocyte HSPB1 increased MI-induced cardiac rupture and mortality within 21 days after MI. Serial echocardiography showed more aggravated remodelling and cardiac dysfunction in Hspb1-/- mice than in WT mice at 1, 3, and 7 days after MI. Decreased collagen deposition and angiogenesis, as well as increased MMP2 and MMP9 activity, were also observed in Hspb1-/- mice compared with WT controls after MI, using immunofluorescence, polarized light microscopy, and zymographic analyses. Notably, Hspb1-/- hearts exhibited enhanced and prolonged leucocyte infiltration, enhanced expression of inflammatory cytokines, and enhanced TLR4/MyD88/NFκB activation compared with WT controls after MI. In-depth molecular analyses in both mice and primary cardiomyocytes demonstrated that cardiomyocyte-specific knockout of HSPB1 increased nuclear factor-κB (NFκB) activation, which promoted the expression of proinflammatory mediators. This led to increased leucocyte recruitment, thereby to excessive inflammation, ultimately resulting in adverse remodelling, cardiac dysfunction, and cardiac rupture following MI. Conclusion: These data suggest that HSPB1 acts as a negative regulator of NFκB-mediated leucocyte recruitment and the subsequent inflammation in cardiomyocytes. Cardiomyocyte HSPB1 is required for wound healing after MI and could be a target for myocardial repair in MI patients.
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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.