Publications by authors named "J Mercadier"
Background: The heart expresses 2 main subtypes of cAMP-dependent protein kinase (PKA; type I and II) that differ in their regulatory subunits, RIα and RIIα. Embryonic lethality of RIα knockout mice limits the current understanding of type I PKA function in the myocardium. The objective of this study was to test the role of RIα in adult heart contractility and pathological remodeling.
View Article and Find Full Text PDFWe experimentally study the synchronization of chaos generated by semiconductor lasers in a cascade injection configuration, i.e., a tunable master laser is used to generate chaos by optical injection in a transmitter laser that injects light into a receiver laser.
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- Left ventricular remodeling (LVR) after a heart attack (myocardial infarction) can cause serious complications like heart failure and death; the study aims to identify negative LVR patterns 6 months post-MI and how they relate to patient outcomes.
- A multicenter analysis of 410 patients revealed significant increases in heart volume measurements, with around half showing concerning LV dilation, and 37% having a reduced ejection fraction at the 6-month mark.
- Predictive factors for adverse LVR included specific heart function metrics rather than standard clinical characteristics; there was a strong correlation between significant LV changes and increased risk for death or heart failure in the long term.
Dual effect of cardiac FKBP12.6 overexpression on excitation-contraction coupling and the incidence of ventricular arrhythmia depending on its expression level.
J Mol Cell Cardiol
March 2024
FKBP12.6, a binding protein to the immunosuppressant FK506, which also binds the ryanodine receptor (RyR2) in the heart, has been proposed to regulate RyR2 function and to have antiarrhythmic properties. However, the level of FKBP12.
View Article and Find Full Text PDFBackground: Myocardial infarction (MI) induces a repair response that ultimately generates a stable fibrotic scar. Although the scar prevents cardiac rupture, an excessive profibrotic response impairs optimal recovery by promoting the development of noncontractile fibrotic areas. The mechanisms that lead to cardiac fibrosis are diverse and incompletely characterized.
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