Cypa
心力衰竭
肌肉肥大
收缩性
细胞外基质
心功能曲线
细胞外
心肌病
心肌细胞
亲环素A
生物
内科学
医学
细胞生物学
分子生物学
作者
Manuel Sigle,Anne‐Katrin Rohlfing,Melanie Cruz Santos,Timo Kopp,Konstantin Krutzke,Vincent Gidlund,Ferdinand Kollotzek,Julia Marzi,Saskia von Ungern‐Sternberg,Antti Poso,Mathias Heikenwälder,Katja Schenke‐Layland,Peter Seizer,Julia Möllmann,Nikolaus Marx,Robert Feil,Susanne Feil,Robert Łukowski,Oliver Borst,Tilman E. Schäffer,K. Müller,Meinrad Gawaz,David Heinzmann
标识
DOI:10.1161/circresaha.124.324812
摘要
Cardiac hypertrophy is characterized by remodeling of the myocardium, which involves alterations in the ECM (extracellular matrix) and cardiomyocyte structure. These alterations critically contribute to impaired contractility and relaxation, ultimately leading to heart failure. Emerging evidence implicates that extracellular signaling molecules are critically involved in the pathogenesis of cardiac hypertrophy and remodeling. The immunophilin CyPA (cyclophilin A) has been identified as a potential culprit. In this study, we aimed to unravel the interplay between eCyPA (extracellular CyPA) and myocardial dysfunction and evaluate the therapeutic potential of inhibiting its extracellular accumulation to improve heart function.
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