Reactive Oxygen Species (ROS) in Metabolic Disease—Don’t Shoot the Metabolic Messenger DOI Open Access
Ross T. Lindsay, Christopher J. Rhodes

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(6), С. 2622 - 2622

Опубликована: Март 14, 2025

Reactive oxygen species (ROS) are widely considered key to pathogenesis in chronic metabolic disease. Consequently, much attention is rightly focused on minimising oxidative damage. However, for ROS production be most effectively modulated, it crucial first appreciate that do not solely function as pathological mediators. There >90 gene products specifically evolved generate, handle, and tightly buffer the cellular concentration of ROS. Therefore, likely plays a role integral homeostatic signalling components only become toxic extremis. This review explores these commonly overlooked normal physiological functions, including how generated response environmental or hormonal stimuli, mechanisms by which signals propagated regulated, cell brings signal an end after appropriate duration. In course this, several specific better-characterised rely upon explored, threshold at cross from beneficial molecules pathology mediators discussed.

Язык: Английский

Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis DOI Creative Commons
Jiayin Wang, Dandan Jia, Zhiwang Zhang

и другие.

Metabolites, Год журнала: 2025, Номер 15(1), С. 59 - 59

Опубликована: Янв. 16, 2025

Background/Objectives: Sarcopenia, characterized by the progressive loss of muscle mass and strength, is linked to physical disability, metabolic dysfunction, an increased risk mortality. Exercise therapy currently acknowledged as a viable approach for addressing sarcopenia. Nevertheless, molecular mechanisms behind exercise training or activity remain poorly understood. The disruption mitochondrial homeostasis implicated in pathogenesis effectively delays onset sarcopenia significantly maintaining homeostasis, including promoting mitophagy, improving biogenesis, balancing dynamics, redox. Exerkines (e.g., adipokines, myokines, hepatokines, osteokines), signaling molecules released response training, may potentially contribute skeletal metabolism through ameliorating reducing inflammation, regulating protein synthesis defense against Methods: In this review, we provide detailed summary exercise-induced exerkines confer their benefit, with particular focus on impact context Results: induces substantial adaptations muscle, mass, improved regeneration hypertrophy, elevated hormone release, enhanced function. An expanding body research highlights that have potential regulate processes such autophagy, redox balance. These maintenance thereby supporting health. Conclusions: Through comprehensive investigation within mitochondria, reveals new insights into key exercise-protective sensors combating

Язык: Английский

Процитировано

1

Reactive Oxygen Species (ROS) in Metabolic Disease—Don’t Shoot the Metabolic Messenger DOI Open Access
Ross T. Lindsay, Christopher J. Rhodes

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(6), С. 2622 - 2622

Опубликована: Март 14, 2025

Reactive oxygen species (ROS) are widely considered key to pathogenesis in chronic metabolic disease. Consequently, much attention is rightly focused on minimising oxidative damage. However, for ROS production be most effectively modulated, it crucial first appreciate that do not solely function as pathological mediators. There >90 gene products specifically evolved generate, handle, and tightly buffer the cellular concentration of ROS. Therefore, likely plays a role integral homeostatic signalling components only become toxic extremis. This review explores these commonly overlooked normal physiological functions, including how generated response environmental or hormonal stimuli, mechanisms by which signals propagated regulated, cell brings signal an end after appropriate duration. In course this, several specific better-characterised rely upon explored, threshold at cross from beneficial molecules pathology mediators discussed.

Язык: Английский

Процитировано

0