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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11152971PMC
http://dx.doi.org/10.1016/j.ijcrp.2024.200284DOI Listing

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From Ca dysregulation to heart failure: β-adrenoceptor activation by RKIP postpones molecular damages and subsequent cardiac dysfunction in mice carrying mutant PLN by correction of aberrant Ca-handling.

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December 2024

Institute of Pharmacology and Toxicology, University of Würzburg, Versbacher Str. 9, 97078 Würzburg, Germany; Leibniz-Institut für Analytische Wissenschaften - ISAS - e.V., Bunsen-Kirchhoff-Str. 11, 44139 Dortmund, Germany; Comprehensive Heart Failure Center, University Hospital of Würzburg, Am Schwarzenberg 15, 97078 Würzburg, Germany. Electronic address:

Article Synopsis
  • Impaired calcium (Ca) handling in heart cells is a key feature of heart failure (HF), leading to issues like weakened heart contractions and irregular heartbeats.
  • The study used transgenic mice with a mutation affecting a calcium regulator (phospholamban) to understand how defects in calcium cycling contribute to HF, noting that these mice experience severe and fast-progressing heart failure.
  • Early treatment aimed at correcting calcium cycling using Raf kinase inhibitor protein (RKIP) was found to delay heart cell damage and improve overall health of the mice, indicating that addressing Ca dynamics early on could be crucial for preventing further complications in heart failure.
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Materials And Methods: A total of 600 patients with pseudonormal LVDFP and preserved EF who underwent follow-up echocardiography were enrolled between 2011 and 2020.

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Cardiomyopathies, historically regarded as rare, are increasingly recognized due to advances in imaging diagnostics and heightened clinical focus. These conditions, characterized by structural and functional abnormalities of the myocardium, pose significant challenges in both chronic and acute patient management. A thorough understanding of the hemodynamic properties, specifically the pressure-volume relationships, is essential.

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Introduction: Preeclampsia (PE) is thought to be the consequence of impaired placental perfusion leading to placental hypoxia. While it has been demonstrated that PE may be a consequence of maternal cardiovascular maladaptation, the exact role of maternal cardiac function remains to be determined. This study sought to assess cardiac characteristics in pregnant women diagnosed with PE and to determine the possible relationship between PE, maternal cardiac changes/function, and NT-proBNP levels.

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