Relaxin and extracellular matrix remodeling: Mechanisms and signaling pathways.
Mol Cell Endocrinol
; 487: 59-65, 2019 05 01.
Article
in En
| MEDLINE
| ID: mdl-30660699
ABSTRACT
Fibrosis is associated with accumulation of excess fibrillar collagen, leading to tissue dysfunction. Numerous processes, including inflammation, myofibroblast activation, and endothelial-to-mesenchymal transition, play a role in the establishment and progression of fibrosis. Relaxin is a peptide hormone with well-known antifibrotic properties that result from its action on numerous cellular targets to reduce fibrosis. Relaxin activates multiple signal transduction pathways as a mechanism to suppress inflammation and myofibroblast activation in fibrosis. In this review, the general mechanisms underlying fibrotic diseases are described, along with the current state of knowledge regarding cellular targets of relaxin. Finally, an overview is presented summarizing the signaling pathways activated by relaxin and other relaxin family peptide receptor agonists to suppress fibrosis.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Relaxin
/
Signal Transduction
/
Extracellular Matrix
Limits:
Animals
/
Humans
Language:
En
Journal:
Mol Cell Endocrinol
Year:
2019
Document type:
Article