Key result
Genetic mouse models confirm the TGF-beta/TAK1 pathway is involved in cardiac hypertrophy and fibrosis, while Smad-dependent signalling may be inhibitory for cardiac hypertrophy.
Genetic mouse models reveal that the TGF-beta/TAK1 pathway drives cardiac hypertrophy and fibrosis, whereas Smad-dependent signaling may be inhibitory.
Requires human validation before targeting TGF-beta/TAK1 in hypertrophy; leaves open clinical translation of mouse findings.
In the present review, we focus on the genetic mouse models for transforming growth factor (TGF)-beta signalling, which have aided our understanding on the role of the TGF-beta signalling pathway in cardiac hypertrophy/fibrosis and the molecular mechanisms involved. 2. Knockout of TGF-beta is embryonic lethal, indicating that TGF-beta signalling plays an important role in embryonic development. In order to avoid this defect, many mouse strains with cardiac-specific targeted genes in TGF-beta signalling have been developed. 3. The TGF-beta family signalling pathway includes Smad-dependent and -independent pathways. 4. Investigations using the genetic mouse models have confirmed and uncovered the involvement of the TGF-beta/TGF-beta-activated kinase 1 (TAK1) pathway in the development of cardiac hypertrophy and fibrosis. Although the downstream cascade of TAK1-induced cardiac hypertrophy remains only partially defined, recent research indicates that the TGF-beta/TAK1/p38 pathway is involved in cardiac fibrosis 5. Smad-dependent signalling may not be involved in, or may even be inhibitory for, cardiac hypertrophy.
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Xiao et al. (2008) conducted a review in Cardiac hypertrophy and fibrosis. Transforming growth factor (TGF)-beta signalling was evaluated. Genetic mouse models confirm the TGF-beta/TAK1 pathway is involved in cardiac hypertrophy and fibrosis, while Smad-dependent signalling may be inhibitory for cardiac hypertrophy.
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