The heart is one of the least regenerative organs in mammals. Damage to heart tissue, such as that resulting from a heart attack, produces a harmful inflammatory response and the formation of scar tissue rather than regeneration. Scarring disrupts normal tissue function, whether in the heart or elsewhere. The research community would like to suppress the unhelpful inflammation and scarring following injury in all types of tissue, but this phenomenon is particular problematic in the heart. Here, researchers demonstrate that the source of this inflammation may be largely the activity of B cells.
In a heart attack, blood is cut off from an area of the heart that then often dies. If the person survives, the body tries to heal the dead muscle by forming scar tissue – but such tissue can further weaken the heart. Yet another wave of damage can occur when well-intentioned immune cells try to heal the injured heart but instead drive inflammation. Pirfenidone is approved to treat a lung condition called idiopathic pulmonary fibrosis, a scarring of the lungs that has no known cause. The drug also has been known for its heart-protective effects in a number of different animal models of heart
Article originally posted at