ArticleESC heart failure2020
Loss of myeloid differentiation protein 1 promotes atrial fibrillation in heart failure with preserved ejection fraction.
Article in ESC heart failure, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Review
- Cardiovascular, Kidney, Liver, and Metabolic Interactions in Heart Failure: Breaking Down Silos.Circulation research · 2025Review
- Identification of common signature genes and pathways underlying the pathogenesis association between nonalcoholic fatty liver disease and heart failure.Frontiers in immunology · 2024Article
- Deficiency of inhibitory TLR4 homolog RP105 exacerbates fibrosis.JCI insight · 2022Article
- Genomic, Proteomic, and Metabolic Comparisons of Small Animal Models of Heart Failure With Preserved Ejection Fraction: A Tale of Mice, Rats, and Cats.Journal of the American Heart Association · 2022Review
- Skeletal muscle phenotypic switching in heart failure with preserved ejection fraction.Frontiers in cardiovascular medicine · 2022Article
- Ferrostatin-1 alleviates lipopolysaccharide-induced cardiac dysfunction.Bioengineered · 2021Article
- Review
- The Akt pathway mediates the protective effects of myeloid differentiation protein 1 in pathological cardiac remodelling.ESC heart failure · 2021Article
- The Potential Role of RP105 in Regulation of Inflammation and Osteoclastogenesis During Inflammatory Diseases.Frontiers in cell and developmental biology · 2021Review
- Loss of myeloid differentiation protein 1 promotes atrial fibrillation in heart failure with preserved ejection fraction.ESC heart failure · 2020Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
aimsMyeloid differentiation protein 1 (MD1) is expressed in the mammalian heart and exerts an anti-arrhythmic effect. Atrial fibrillation (AF) is closely related to heart failure with preserved ejection fraction (HFpEF). The potential impact of MD1 on AF vulnerability in an HFpEF model is not clear. METHODS AND
resultsMD1 knock-out and wild-type (WT) mice were subjected to uninephrectomy and continuous saline or d-aldosterone infusion and given 1% sodium chloride drinking water for 4 weeks. Echocardiographic and haemodynamic measurements, electrophysiological studies, Masson staining, and molecular analysis were performed. Aldosterone-infused WT mice develop HFpEF with left ventricular hypertrophy, moderate hypertension, pulmonary congestion, and diastolic dysfunction. Aldosterone infusion increased the vulnerability of WT mice to AF, as shown by a prolonged interatrial conduction time, shortened effective refractory period, and higher incidence of AF. In addition, aldosterone infusion increased myocardial fibrosis and inflammation, decreased sarcoplasmic reticulum Ca
conclusionsMD1 deficiency increases the vulnerability of HFpEF mice to AF. This is mainly caused by aggravated maladaptive left atrial fibrosis and inflammation and worsened dysregulation of calcium handling, which is induced by the enhanced activation of the toll-like receptor 4/calmodulin-dependent protein kinase II signalling pathway.
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