It has been postulated that quiescence protects stem cells from incurring damage during cell division and plays a necessary role in their lifetime maintenance. The few exceptions, such as intestinal stem cells ( 97), are the subject of debate ( 72, 87). ROS damage is also known to contribute to inflammation however, the cross-talk between ROS and the inflammatory response in stem cells is unclear.Īdult stem cells are known to be mostly quiescent and to rarely enter cell cycle ( 38). In turn, these diseases can lead to further dysregulation of ROS signaling and increased oxidative stress. Oxidative stress and aberrant ROS signaling are associated with aging-related diseases including cancer. 20, 1902–1916.Ĭontribution of ROS to disease in stem cells. Future Directions: Future work in elucidating how ROS control stem cell cycling, apoptotic machinery, and lineage determination should shed light on mechanisms whereby ROS may control stem cell aging. In general, based on the work described here we propose a model in which ROS function as stem cell rheostat. We will specifically focus on how alterations in this regulation may be implicated in disease and particularly in diseases of stem cell aging. Critical Issues: Here we review recent published work on major signaling pathways and transcription factors that are regulated by ROS and mediate ROS regulation of stem cell fate. ![]() Although reactive oxygen species (ROS) are better known for their damaging properties to DNA, proteins and lipids, recent findings suggest that ROS may also be an integral physiological mediator of cellular signaling in primary cells. Recent Advances: Recent findings implicate redox metabolism in the control of stem cell pool and stem cell aging. Significance: Functional stem cell decline has been postulated to result in loss of maintenance of tissue homeostasis leading to organismal decline and diseases of aging.
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