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Several of these mouse models exhibit aspects of HCV-related liver disease.
ALDH2*2 mouse models exhibit osteoblastic dysfunction due to oxidative stress mediated by accumulated acetaldehyde levels in the absence of alcohol intake23.
However, many of these mouse models exhibit slow progressive axonal loss which can span over many months.
Both mouse models exhibit increased prostatic branching.
Indeed, EGFL7 loss-of-function mouse models exhibit partial embryonic lethality and serious vascular abnormalities [ 7].
Down syndrome (DS) mouse models exhibit cognitive deficits, and are used for studying the neuronal basis of DS pathology.
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Also, an increased proportion of alpha-cells within the central core is observed in the pancreas of mouse models exhibiting increased demand for insulin.
Consistent with this, adenosine levels are elevated in various mouse models exhibiting features of chronic lung disease [23], [24], [25], [26].
Another apparent conflict appears in the mouse models exhibiting hypersecretion and decreased β cell mass.
Mouse models exhibiting overexpression of Wnt ligands are also not readily available.
Dry skin mouse models exhibited sensitization to PAR2 agonists and a PAR2 antibody helped reduce scratching [ 125].
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