ALL STEM CELLS

eart attacks caused by a blockage in the coronary artery induce severe injury to cardiac muscle cells, leading to cell dysfunction and death. The damage elicits repair and regenerative responses that provoke the removal of dying cells and cell debris, recruit immune cells and initiate the formation of new blood vessels to recover blood supply. Fibroblast cells play a central part in this repair response. In this issue, Ubil et al. describe how the plasticity of cardiac fibroblasts contributes to this process, by showing that fibroblasts can, in response to the activity of the transcription factor, convert into the endothelial cells that line the interior surface of blood vessels.
The heart consists of myocytes (muscle cells) and non-myocytes, which include cardiac fibroblasts and endothelial cells. The fibroblasts produce growth factors and extracellular matrix (ECM) proteins to maintain proper cardiac architecture, contraction and function. They also interact with endothelial cells and myocytes to aid angiogenesis (bloodvessel formation) and maintain physiological homeostasis. Following heart damage, cardiac fibroblasts are activated to produce ECM proteins and soluble factors to compensate for structural defects, contain the spread of damage, reinforce cardiac stiffness and prevent cardiac rupture. These activities, collectively referred to as fibrosis, aid in remodeling the heart musculature. Controlled fibrosis is crucial for restoring cardiac function after injury.
However, excessive fibrosis is considered a pathological process that can lead to adverse effects, including reduced cardiac stiffness (diastolic dysfunction) and irregular electrical connectivity (arrhythmia).

See More : Nature.com (15 October 2014)