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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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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:
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- 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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Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
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