We used a set of transgenic Drosophila based on the well-characterized temperature-sensitive Gal80 protein (Gal80ts) in the context of the bipartite Gal4/UAS transgenic expression system in Drosophila employing the cardiac specific driver, tinCΔ4-Gal4.
We engineered transgenic Drosophila based on the well-characterized temperature-sensitive Gal80 protein in the context of the bipartite Gal4/UAS transgenic expression system in Drosophila employing the cardiac specific driver, tinCΔ4-Gal4.
Cardiac-specific driver hand- Gal4 and cardiomyocyte-specific driver GMH5 have been previously described (Wessells et al., 2004; Han & Olson, 2005).
The NTD Chagas disease is a driver of cardiac myopathy, for instance, and schistosomiasis pre-disposes to bladder cancer.
In sheep before 100 days gestation (term, 150 ± 3 d gestation) all cardiomyocytes in the heart of the fetus are mononucleated and capable of proliferation, thereafter binucleation begins and hypertrophy becomes the predominant driver of cardiac growth [ 32, 33].
This is accompanied by marked changes in cardiomyocyte biology and myocardial inflammation, which is a key driver of cardiac remodelling in this setting, particularly in regard to the ECM [ 8, 16, 46].
From a clinical perspective, much attention has focused on the concept that oxidative stress may be a driver of cardiac disease progression (e.g., heart failure) but clinical interventions with antioxidants have had little or no impact on heart disease risk and progression.
Although these findings merit further investigation, they show the capability of WNC scores to recognize known drivers of cardiac regeneration and possible novel candidates.
Notably, in addition to our previous work highlighting macrophage-specific effects of exendin-4 post-MI [ 34], many basic and clinical studies are broadly supportive of persistent anti-inflammatory actions of GLP-1, including specific reduction of TNF-α, IL-6, TLR-2/4, NF-κβ, and MMP-9, which are key drivers of cardiac remodelling [ 9, 17, 40].
Cardiac infiltration is the chief driver of prognosis in systemic amyloidosis.
