# In Vitro Antioxidant Effects of Coenzyme Q10 on Cellular Metabolism in Aged Mesenchymal Stem Cells
## 1 Introduction  
Stem cell aging is a key process in understanding organismal aging. Adult stem cells found in various tissues are essential for organ-specific regeneration, self-renewal, and tissue maintenance, particularly as the body ages [1]. Their functionality plays a vital role in organ-specific regeneration and self-renewal, particularly as the body ages or upon exposure to tissue damage causing agents [2]. Tissue maintenance and regeneration rely heavily on the presence and functionality of stem cells. Consequently, age-related declines in stem cell numbers or functionality can significantly impair the body's regenerative capacity, emphasizing their critical role in sustaining tissue health and repair throughout life [3]. Over the years, mesenchymal stem cells (MSCs) have emerged as a promising resource for stem cell-based therapies, with particular emphasis on their potential applications in regenerative medicine as anti-aging treatments. Their exceptional clinical attributes, such as ease of accessibility, simple isolation procedures, robust self-renewal and proliferation capacity, multilineage differentiation potential, and immunomodulatory properties, make them highly promising [1]. However, numerous studies have demonstrated that MSCs experience functional decline and progressive loss of stemness with advancing age in vivo or during extended in vitro culture [3; 4; 5]. These age-related changes significantly constrain their therapeutic applications. While the mechanisms underlying MSC senescence remain incompletely understood, considerable progress has been made in identifying age-associated phenotypic alterations and uncovering the potential molecular pathways contributing to MSC aging. This growing body of knowledge offers valuable insights in overcoming the limitations of MSC-based therapies and enhancing their clinical usability [1]. Aging is associated with a pro-oxidizing shift in the cellular redox state, coupled with the accumulation of oxidatively damaged biomolecules. Together, these factors are believed to contribute causally to cellular senescence [6]. This concept, often referred to as the oxidative stress hypothesis, posits that aging involves an imbalance between pro-oxidant production and antioxidant cellular defenses, leading to an increased oxidant load or stress. Mitochondria are considered to play a central role in this dysregulation, as they are major sources of reactive oxygen species (ROS). During aging, mitochondrial ROS production (primarily O2\({}^{-}\) and H2O2) increases, accompanied by oxidative damage to mitochondrial DNA, proteins, and lipids [6; 7]. A critical consequence of this damage is a self-perpetuating cycle in which oxidative injury accelerates the rate of ROS generation, a phenomenon first described by [PERSON] and colleagues [8]. Another significant age-related mitochondrial alteration is the decline in ADP-stimulated (state 3) and maximal (uncoupled) rates of mitochondrial oxygen consumption [9]. These changes, combined with increased oxidative stress and damage from elevated O2\({}^{-}\)/H2O2 production and a diminished mitochondrial capacity to synthesize ATP, are believed to progressively impair the functional capacity of various physiological systems [6]. Coenzyme Q10 (CoQ10) is a lipophilic redox-active molecule primarily localized within the inner mitochondrial membrane, where it plays a pivotal role in cellular energy production. It is also integrated into the phospholipid bilayer of various cellular membranes, where it helps modulate their physicochemical properties [10]. CoQ10 is particularly concentrated in the mitochondria, highlighting its essential function in oxidative phosphorylation and electron transport processes [4]. As a vital component of the electron transport chain, CoQ10 directly participates in oxidative phosphorylation, enabling efficient energy production [11].