Key result
TGFbeta acts as a major pro-fibrotic cytokine in cardiac fibrosis, presenting several potential signaling pathways as targets for selective drug intervention against chronic fibrotic disease.
This review highlights the role of TGFbeta in cardiac fibrosis and identifies potential signaling pathways for selective anti-fibrotic drug interventions.
Pathway-specific TGFbeta inhibition may limit fibrosis with fewer off-target effects; leaves open validation of cardiac-relevant targets in clinical studies.
The cytokine transforming growth factor beta (TGFbeta) is a major contributor to fibrogenic responses both in vitro and in vivo. TGFbeta possesses many functions; thus, broadly targeting TGFbeta signaling as an anti-fibrotic approach is anticipated to be problematic. Recent experiments, however, have begun to elucidate the signaling pathways through which TGFbeta activates a fibrotic program. This review critically evaluates the evidence supporting TGFbeta as a pro-fibrotic cytokine, with special attention to cardiac fibrosis, and suggests several possible points for selective drug intervention to combat chronic fibrotic disease.
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Andrew Leask (2006) conducted a review in Cardiac fibrosis. TGFbeta signaling was evaluated. TGFbeta acts as a major pro-fibrotic cytokine in cardiac fibrosis, presenting several potential signaling pathways as targets for selective drug intervention against chronic fibrotic disease.
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