Key result
Cardiac-specific overexpression of p38 MAPK in rats upregulated 264 genes more than 2-fold, leading to myocardial cell proliferation, inflammation, and fibrosis.
Population
Rats (in vivo model)
Design
Preclinical
Authors
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Suggests p38 MAPK drives rodent myocardial fibrosis; leaves open its therapeutic targeting in human heart disease.
In vivo overexpression of p38 MAPK in the rat heart identifies its role in upregulating cell cycle and inflammatory genes, driving pathological myocardial proliferation and fibrosis.
Tenhunen et al. (2006) studied this question. Adenovirus-mediated gene transfer of MKK3bE and wild-type p38alpha was evaluated on Gene expression profile and functional effects. Cardiac-specific overexpression of p38 MAPK in rats upregulated 264 genes more than 2-fold, leading to myocardial cell proliferation, inflammation, and fibrosis.
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