Targeting TGF-β signaling for the treatment of fibrosis
Transforming growth factor-β (TGF-β) is widely recognized as a core pathway of fibrosis.
Inhibition of TGF-β signaling may thus offer potential for antifibrotic therapies. Long-term
inhibition of TGF-β signaling at the level of its isoforms and receptors can be associated with
unacceptable adverse effects. However, TGF-β regulates a myriad of intracellular signaling
cascades to transmit its profibrotic effects and several of those pathways offer potential for
pharmacologic intervention. Moreover, the multiple interactions of TGF-β with other …
Inhibition of TGF-β signaling may thus offer potential for antifibrotic therapies. Long-term
inhibition of TGF-β signaling at the level of its isoforms and receptors can be associated with
unacceptable adverse effects. However, TGF-β regulates a myriad of intracellular signaling
cascades to transmit its profibrotic effects and several of those pathways offer potential for
pharmacologic intervention. Moreover, the multiple interactions of TGF-β with other …
Abstract
Transforming growth factor-β (TGF-β) is widely recognized as a core pathway of fibrosis. Inhibition of TGF-β signaling may thus offer potential for antifibrotic therapies. Long-term inhibition of TGF-β signaling at the level of its isoforms and receptors can be associated with unacceptable adverse effects. However, TGF-β regulates a myriad of intracellular signaling cascades to transmit its profibrotic effects and several of those pathways offer potential for pharmacologic intervention. Moreover, the multiple interactions of TGF-β with other profibrotic pathways also yielded candidates for therapeutic intervention. In this review, we discuss selected targets within the TGF-β pathway with high translational potential.
Elsevier