In fibrosis, the unregulated differentiation of wound healing fibroblasts into myofibroblasts is assumed to be a critical step on the development of fibrotic disorders. In this context, GPCRs are especially investigated under the hypothesis that some of them may have profibrotic or antifibrotic effects by regulating the differentiation of fibroblasts into myofibroblasts. The diverse and dynamic expression of GPCRs in cells adds a layer of complexity to the understanding of their roles in fibrosis.
In this review, you will:
- Identify GPCR receptors having signaling abilities that inhibits pro-fibrotic hallmarks like the differentiation and proliferation of fibroblasts
- Better understand the ties between the anti-fibrotic effects of relaxin and ATR2
- Explore the functional interactions between the angiotensin II (AngII) and CCL2 receptors (AT1R & CCR2)
