Cardiac robustness regulated by reactive sulfur species

  • Nishimura Akiyuki
    National Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences Exploratory Research Center on Life and Living Systems (ExCELLS), National Institutes of Natural Sciences SOKENDAI (School of Life Science, The Graduate University for Advanced Studies)
  • Tanaka Tomohiro
    National Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences Exploratory Research Center on Life and Living Systems (ExCELLS), National Institutes of Natural Sciences SOKENDAI (School of Life Science, The Graduate University for Advanced Studies) Center for Novel Science Initiatives (CNSI), National Institutes of Natural Sciences
  • Kato Yuri
    Department of Physiology, Graduate School of Pharmaceutical Sciences, Kyushu University
  • Nishiyama Kazuhiro
    Department of Physiology, Graduate School of Pharmaceutical Sciences, Kyushu University
  • Nishida Motohiro
    National Institute for Physiological Sciences (NIPS), National Institutes of Natural Sciences Exploratory Research Center on Life and Living Systems (ExCELLS), National Institutes of Natural Sciences SOKENDAI (School of Life Science, The Graduate University for Advanced Studies) Center for Novel Science Initiatives (CNSI), National Institutes of Natural Sciences Department of Physiology, Graduate School of Pharmaceutical Sciences, Kyushu University

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<p>The human myocardium contains robust cells that constantly beat from birth to death without being replaced, even when exposed to various environmental stresses. Myocardial robustness is thought to depend primarily on the strength of the reducing power to protect the heart from oxidative stress. Myocardial antioxidant systems are controlled by redox reactions, primarily via the redox reaction of Cys sulfhydryl groups, such as found in thioredoxin and glutathione. However, the specific molecular entities that regulate myocardial reducing power have long been debated. Recently, reactive sulfide species, with excellent electron transfer ability, consisting of a series of multiple sulfur atoms, i.e., Cys persulfide and Cys polysulfides, have been found to play an essential role in maintaining mitochondrial quality and function, as well as myocardial robustness. This review presents the latest findings on the molecular mechanisms underlying mitochondrial energy metabolism and the maintenance of quality control by reactive sulfide species and provides a new insight for the prevention of chronic heart failure.</p>

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