ArticleInternational journal of molecular sciences2020
Structural, Pro-Inflammatory and Calcium Handling Remodeling Underlies Spontaneous Onset of Paroxysmal Atrial Fibrillation in JDP2-Overexpressing Mice.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 12 citations in OpenAlex.
- The Defect of iNKT Cells Mediates Mitochondrial Dysfunction Through IL-6/STAT3 Signaling to Induce Atrial Inflammation and Fibrosis to Aggravate Postoperative Atrial Fibrillation.Physiological research · 2026Article
- Maintenance and Reversibility of Paroxysmal Atrial Fibrillation in JDP2 Overexpressing Mice.Cells · 2025Article
- Atrial fibrillation risk model based on LASSO and SVM algorithms and immune infiltration of key mitochondrial energy metabolism genes.Scientific reports · 2025Article
- Identification and characterization of novel ferroptosis-related genes in acute myocardial infarction.Human genomics · 2024Article
- Amlexanox reduces new-onset atrial fibrillation risk in sepsis by downregulating S100A12: a Mendelian randomization study.Frontiers in cardiovascular medicine · 2024Article
- Establishment of Risk Model and Analysis of Immunoinfiltration Based on Mitophagy-Related Associated Genes in Atrial Fibrillation.Journal of inflammation research · 2023Article
- Animal models and animal-free innovations for cardiovascular research: current status and routes to be explored. Consensus document of the ESC Working Group on Myocardial Function and the ESC Working Group on Cellular Biology of the Heart.Cardiovascular research · 2022Article
- Animal Models to Study Cardiac Arrhythmias.Circulation research · 2022Review
- Mechanisms Underlying Antiarrhythmic Properties of Cardioprotective Agents Impacting Inflammation and Oxidative Stress.International journal of molecular sciences · 2022Review
- JDP2, a Novel Molecular Key in Heart Failure and Atrial Fibrillation?International journal of molecular sciences · 2021Review
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9 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundCardiac-specific JDP2 overexpression provokes ventricular dysfunction and atrial dilatation in mice. We performed in vivo studies on JDP2-overexpressing mice to investigate the impact of JDP2 on the predisposition to spontaneous atrial fibrillation (AF).
methodsJDP2-overexpression was started by withdrawal of a doxycycline diet in 4-week-old mice. The spontaneous onset of AF was documented by ECG within 4 to 5 weeks of JDP2 overexpression. Gene expression was analyzed by real-time RT-PCR and Western blots.
resultsIn atrial tissue of JDP2 mice, besides the 3.6-fold increase of JDP2 mRNA, no changes could be detected within one week of JDP2 overexpression. Atrial dilatation and hypertrophy, combined with elongated cardiomyocytes and fibrosis, became evident after 5 weeks of JDP2 overexpression. Electrocardiogram (ECG) recordings revealed prolonged PQ-intervals and broadened P-waves and QRS-complexes, as well as AV-blocks and paroxysmal AF. Furthermore, reductions were found in the atrial mRNA and protein level of the calcium-handling proteins NCX, Cav1.2 and RyR2, as well as of connexin40 mRNA. mRNA of the hypertrophic marker gene ANP, pro-inflammatory MCP1, as well as markers of immune cell infiltration (CD68, CD20) were increased in JDP2 mice.
conclusionJDP2 is an important regulator of atrial calcium and immune homeostasis and is involved in the development of atrial conduction defects and arrhythmogenic substrates preceding paroxysmal AF.
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