title: Redox signaling in cardiac renewal.
abstract: CONCLUSIONS
  Utilizing oxygen (O2) through mitochondrial oxidative phosphorylation enables organisms to generate adenosine triphosphate (ATP) with a higher efficiency than glycolysis, but it results in increased reactive oxygen species production from mitochondria, which can result in stem cell dysfunction and senescence.
  
  
  BACKGROUND
  In the postnatal organism, the hematopoietic system represents a classic example of the role of stem cells in cellular turnover and regeneration. However, in other organs such as the heart, both the degree and source of cellular turnover have been heavily contested.
  
  
  RESULTS
  Although recent evidence suggests that the major source of the limited cardiomyocyte turnover in the adult heart is cardiomyocyte proliferation, the identity and potential role of undifferentiated cardiac progenitor cells remain controversial. Several types of cardiac progenitor cells have been identified, and several studies have identified an important role of redox and metabolic regulation in survival and differentiation of cardiac progenitor cells. Perhaps a simple way to approach these controversies is to focus on the multipotentiality characteristics of a certain progenitor population, and not necessarily its ability to give rise to all cell types within the heart. In addition, it is important to note that cycling cells in the heart may express markers of differentiation or may be truly undifferentiated, and for the purpose of this review, we will refer to these cycling cells as progenitors.
  
  
  CONCLUSIONS
  We propose that hypoxia, redox signaling, and metabolic phenotypes are major regulators of cardiac renewal, and may prove to be important therapeutic targets for heart regeneration.
authors.affiliation: 1 Division of Cardiology, Department of Internal Medicine, UT Southwestern Medical Center , Dallas, Texas.
authors.forename: Wataru
authors.initials: W
authors.lastname: Kimura
authors.forename: Shalini
authors.initials: S
authors.lastname: Muralidhar
authors.forename: Diana C
authors.initials: DC
authors.lastname: Canseco
authors.forename: Bao
authors.initials: B
authors.lastname: Puente
authors.forename: Cheng Cheng
authors.initials: CC
authors.lastname: Zhang
authors.forename: Feng
authors.initials: F
authors.lastname: Xiao
authors.forename: Yezan H
authors.initials: YH
authors.lastname: Abderrahman
authors.forename: Hesham A
authors.initials: HA
authors.lastname: Sadek
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D002454:Cell Differentiation; D060833:Cellular Microenvironment; D006801:Humans; D000860:Hypoxia; D032383:Myocytes, Cardiac / Q000166:cytology* / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism; D012038:Regeneration; D015398:Signal Transduction; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species