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REVIEW article

Front. Cell Dev. Biol.
Sec. Stem Cell Research
Volume 12 - 2024 | doi: 10.3389/fcell.2024.1432668

NOX4-Reactive Oxygen Species Axis: Critical Regulators of Bone Health and Metabolism

Provisionally accepted
  • 1 Laboratory of Molecular Physiology of Bone, Institute of Physiology, Academy of Sciences of the Czech Republic (ASCR), Prague, Prague, Czechia
  • 2 Faculty of Science, Charles University, Prague, Czechia
  • 3 Translational Biology, Medicine and Health, Virginia Tech, Blacksburg, Virginia, United States
  • 4 Department of Human Nutrition, Foods, and Exercise, College of Agriculture and Life Sciences, Virginia Tech, Blacksburg, Virginia, United States

The final, formatted version of the article will be published soon.

    Bone marrow stromal cells (BMSCs) play a significant role in bone metabolism as they can differentiate into osteoblasts, bone marrow adipocytes (BMAds), and chondrocytes. BMSCs chronically exposed to nutrient overload undergo adipogenic programming, resulting in bone marrow adipose tissue (BMAT) formation. BMAT is a fat depot transcriptionally, metabolically, and morphologically distinct from peripheral adipose depots.Reactive oxygen species (ROS) are elevated in obesity and serve as important signals directing BMSC fate. ROS produced by the NADPH oxidase (NOX) family of enzymes, such as NOX4, may be responsible for driving BMSC adipogenesis at the expense of osteogenic differentiation. The dual nature of ROS as both cellular signaling mediators and contributors to oxidative stress complicates their effects on bone metabolism. This review discusses the complex interplay between ROS and BMSC differentiation in the context of metabolic bone diseases.Special attention is paid to the role of NOX4-ROS in regulating cellular processes within the bone marrow microenvironment and potential target in metabolic bone diseases.

    Keywords: Bone marrow stromal cells, bone marrow adipose tissue, ROS, NADPH Oxidase, Bone fragility, Obesity, senescence

    Received: 14 May 2024; Accepted: 29 Jul 2024.

    Copyright: © 2024 Dzubanova, Bond, Craige and Tencerova. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Michaela Tencerova, Laboratory of Molecular Physiology of Bone, Institute of Physiology, Academy of Sciences of the Czech Republic (ASCR), Prague, 142 20, Prague, Czechia

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.