Abstract
Oxidative stress in mitochondria is believed to promote aging. Although passive leakage of electron from the mitochondrial electron transport chain has been considered as a major source of oxidative stress in the heart and the cardiomyocytes therein, enzymes actively producing reactive oxygen species may also exist in mitochondria. We have shown recently that Nox4, a member of the NADPH oxidase family, is localized on intracellular membranes, primarily at mitochondria, in cardiomyocytes. Mitochondrial expression of Nox4 is upregulated by cardiac stress and aging in the heart, where Nox4 could become a major source of oxidative stress. This raises an intriguing possibility that Nox4 may play an important role in mediating aging of the heart. Here we discuss the potential involvement of Nox4 in mitochondrial oxidative stress and aging in the heart.
Highlights
Oxidative stress is defined as an excessive accumulation of reactive oxygen species (ROS) beyond the capacity of antioxidants [1]
Nox4 is localized in the peri-nuclear region, especially in mitochondria, in cardiomyocytes
Due to its close proximity to mitochondrial proteins, ROS generated by Nox4 oxidize mitochondrial proteins, which in turn trigger mitochondrial dysfunction and electron leakage
Summary
Oxidative stress is defined as an excessive accumulation of reactive oxygen species (ROS) beyond the capacity of antioxidants [1]. An emerging hypothesis is that Nox4, a member of the NADPH oxidase family, is localized in mitochondria and actively produces ROS under pathological conditions and during aging [12, 13]. The NADPH oxidase was thought to be a phagocyte-specific enzyme and to play a critical role in mediating bacterial killing by producing a burst of O2[10], until its family protein Nox1 was discovered in smooth muscle cells and colonic epithelium [25].
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