Scientists have found a new way to intervene in the molecular and cellular cascade that causes fibrosis - a condition where the body's natural process of forming scars for wound healing goes into overdrive and causes diseases.
The findings demonstrate a potential novel therapeutic approach to treat fibrotic diseases such as idiopathic pulmonary fibrosis and liver fibrosis.
The research targets a pathway that turns off the trigger for the major molecular mediator of fibrosis, a protein called Transforming Growth Factor (TGF) beta.
This protein is normally present in the body in an inactive state and must be turned on to cause fibrosis. Once activated, TGF beta protein stimulates cells called myofibroblasts to produce excess collagen, which is a principle component of scars.
The researchers showed that removing a gene in the myofibroblasts that makes a specific subset of proteins called alpha v integrins blocks the ability of these cells to trigger activation of TGF beta.
Furthermore, they were able to replicate the effect of the gene deletion by treatment with a small molecule compound, thus opening the door to a potential new therapy for patients.
The small molecule was not only able to prevent fibrosis; it made fibrosis less severe even when the treatment was started after fibrosis had begun, Griggs added.
In tandem with the drug discovery research, scientists working on another part of the study found they could protect mice from pulmonary fibrosis, liver fibrosis and renal fibrosis by deleting a gene that makes the same specific integrins in myofibroblasts that were targeted by the drug.
The study has been published in the advance online issue of Nature Medicine. (ANI)