The restricted regenerative capacity of the mammalian heart remains a perplexing exception. The regenerative response launched by other injured organs involves local populations of self-renewing precursor cells, or recruitment of circulating stem cells to replace or repair the injured areas. In response to functional stress, the heart can increase its muscle mass through cellular hypertrophy, but the damaged heart needs a rapid response to repair damage to the muscle wall and maintain adequate blood flow to the rest of the body. Paradoxically, this most critical organ cannot restore the muscle loss that accompanies myocardial infarction and ischemia-reperfusion injury. Instead, interruption of the coronary blood supply results in apoptosis and fibrotic scar formation at the cost of functional muscle. As a result, the remaining cardiomyocytes undergo cellular hypertrophy, leading to decompensated function and congestive heart failure, an increasingly prevalent disease in the industrialized world.
|Title of host publication||Essentials of Stem Cell Biology: Third Edition|
|Number of pages||9|
|Publication status||Published - 4 Nov 2013|
- Endothelial cells
- Heart regeneration
- Smooth muscle cells