We previously showed that lentiviral delivery of Sema3F to a demyelinated lesion in a different mouse model improved remyelination [ 37], giving confidence in these results; an important factor considering the number of drug targets that look promising in initial publications, but which later fail to be repeated by pharmaceutical companies [ 39].
It was observed, in the mice model, improved motor performance and respiratory function, slower disease progression, and delayed-onset disease [ 260, 261].
This suggests that the biological clarity of the mouse model system improves our ability to identify a common underlying biological response to the formation of the tumor.
The gapmer also decreases r(CUG 960 expression in a DM1 mouse model, significantly improving other DM1-associated defects.
Moreover, in vivo overexpression of TGR5 in a transgenic (TGR5-Tg) mouse model markedly improved glucose tolerance in mice fed a high-fat diet compared with controls.
In the present study, PCF successfully decreased the levels of cytokines and restored Treg/Th17 balance in the asthma mouse model, thus improving airway inflammation and reducing asthma symptoms.
These findings suggest that moderate Opa1 overexpression partially rescues the phenotype of a CI-deficient mouse model by improving cristae morphology.
SIRT1 overexpression in this mouse model also improved learning and memory deficits and deletion of SIRT1 worsened these phenotypes (Donmez et al, 2010).
Supplementation with exogenous creatine in one transgenic mouse model showed improved motor performance, reduced atrophy of neurons, and huntingtin protein aggregates, and an observed increased survival rate or life-span.
In a mouse model, levosimendan improved ventricular function and inhibited cardiomyocyte apoptosis in severe acute experimental coxsackie virus myocarditis and was discussed as a therapeutic option in patients with viral myocarditis [ 29].
