Mitochondrial Peroxiredoxins and Monoamine Oxidase-A: Dynamic Regulators of ROS Signaling in Cardioprotection.

An excessive increase in reactive oxygen species (ROS) levels is one of the main causes of mitochondrial dysfunction. However, when ROS levels are maintained in balance with antioxidant mechanisms, ROS fulfill the role of signaling molecules and modulate various physiological processes. Recent advan...

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Publicado en:Physiological Research Vol. 73; no. 6; pp. 887 - 901
Autores principales: FERKO, Miroslav, ALANOVA, Petra, JANKO, David, OPLETALOVA, Barbora, ANDELOVA, Natalia
Formato: Journal Article
Publicado: Institute of Physiology, Academy of Sciences of the Czech Republic Dec2024
Acceso en línea:Ver este registro en EBSCOhost
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      dt: Dec2024
      vid: 73
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      pub: Institute of Physiology, Academy of Sciences of the Czech Republic
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        atl: Mitochondrial Peroxiredoxins and Monoamine Oxidase-A: Dynamic Regulators of ROS Signaling in Cardioprotection.
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        au:
          FERKO, Miroslav
          ALANOVA, Petra
          JANKO, David
          OPLETALOVA, Barbora
          ANDELOVA, Natalia
        affil: Centre of Experimental Medicine, Institute for Heart Research, Slovak Academy of Sciences, Bratislava, Slovak Republic.
      sug:
      ab: An excessive increase in reactive oxygen species (ROS) levels is one of the main causes of mitochondrial dysfunction. However, when ROS levels are maintained in balance with antioxidant mechanisms, ROS fulfill the role of signaling molecules and modulate various physiological processes. Recent advances in mitochondrial bioenergetics research have revealed a significant interplay between mitochondrial peroxiredoxins (PRDXs) and monoamine oxidase-A (MAO-A) in regulating ROS levels. Both proteins are associated with hydrogen peroxide (H2O2), MAO-A as a producer and PRDXs as the primary antioxidant scavengers of H2O2. This review focuses on the currently available knowledge on the function of these proteins and their interaction, highlighting their importance in regulating oxidative damage, apoptosis, and metabolic adaptation in the heart. PRDXs not only scavenge excess H2O2, but also act as regulatory proteins, play an active role in redox signaling, and maintain mitochondrial membrane integrity. Overexpression of MAO-A is associated with increased oxidative damage, leading to mitochondrial dysfunction and subsequent progression of cardiovascular diseases (CVD), including ischemia/reperfusion injury and heart failure. Considering the central role of oxidative damage in the pathogenesis of many CVD, targeting PRDXs activation and MAO-A inhibition may offer new therapeutic strategies aimed at improving cardiac function under conditions of pathological load related to oxidative damage.
      pubtype: Academic Journal
      doctype: Journal Article
      ougenre: Article
    language: English
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