A new route to the treatment of heart disease has been unveiled by scientists at Johns Hopkins.
They have found through mice studies that blocking the action of a signaling protein deep inside the heart's muscle cells blunts the most serious ill effects of high blood pressure on the heart.
These include heart muscle enlargement, scar tissue formation and loss of blood vessel growth.
Specifically, the team found that their intervention halted transforming growth factor beta (TGF-beta) secretion at a precise location called cell receptor type 2 in cardiac muscle cells.
Blocking its action in this cell type forestalled pathways for hypertrophy, fibrosis, and angiogenesis by stopping the unbridled TGF-beta signaling, which is typically observed in heart failure, in all other non-muscle types of cells in blood vessels and fibrous tissue.
However, blocking TGF-beta signaling in non-muscle cells did not stop disease progression.
The study is believed to show the first evidence of how TGF-beta is stimulated differently by various cell types in the heart and which resulting pathways promote heart failure, the most common kind of heart disease.
The study is forthcoming in the Journal of Clinical Investigation.