Relaxin Regulates Collagen Overproduction Associated with Experimental Progressive Renal Fibrosis

• Published in: Annals of the New York Academy of Sciences Vol. 1041; no. 1; pp. 182 - 184
• Main Authors: SAMUEL, CHRISHAN S., MOOKERJEE, ISHANEE, MASTERSON, ROSEMARY, TREGEAR, GEOFFREY W., HEWITSON, TIM D.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.05.2005
• Subjects: Aging - physiology; Animals; Cells, Cultured; Collagen - antagonists & inhibitors; Collagen - biosynthesis; Collagens; cortical fibroblasts; Degradation; Disease Progression; Etiology; Female; Fibroblasts; Fibrosis; Fibrosis - genetics; Fibrosis - metabolism; Fibrosis - pathology; Gene Expression Regulation - drug effects; gene knockout mice; Hormones; Kidney Diseases - genetics; Kidney Diseases - metabolism; Kidney Diseases - pathology; Male; Mice; Pathways; Rats; relaxin; Relaxin - deficiency; Relaxin - genetics; Relaxin - metabolism; Relaxin - pharmacology; renal fibrosis; Scars; unilateral ureteral obstruction
• ISSN: 0077-8923; 1749-6632
• DOI: 10.1196/annals.1282.026

: Progressive fibrosis due to excess extracellular matrix (primarily collagen) is the final common pathway in all forms of chronic renal disease, regardless of etiology, and leads to tissue dysfunction, when normal tissue is replaced by scar tissue. Emerging work from ourselves and others suggests that the naturally occurring hormone relaxin has the potential to limit renal collagen production and reorganization, while increasing its degradation. The outlined studies demonstrate relaxin's potential as an antifibrotic agent against experimental progressive renal disease.