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Mitochondrial ROS and involvement of Bcl-2 as a mitochondrial ROS regulator
Stephen Jun Fei Chong1, Ivan Cherh Chiet Low1, Shazib Pervaiz2
1Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 10 Medical Drive, Clinical Research Center, #04-25, Singapore 117597, Singapore.
Abstract:
Mitochondria are the major intracellular source of reactive oxygen species (ROS). While excessive mitochondrial ROS (mitoROS) production induces cell injury and death, there is accumulating evidence that non-toxic low levels of mitoROS could serve as important signaling molecules. Therefore, maintenance of mitoROS at physiological levels is crucial for cell homeostasis as well as for survival and proliferation. This review describes the various mechanisms that keep mitoROS in check, with particular focus on the role of the onco-protein Bcl-2 in redox regulation. In addition to its canonical anti-apoptotic activity, Bcl-2 has been implicated in mitoROS regulation by its effect on mitochondrial complex IV activity, facilitating the mitochondrial incorporation of GSH and interaction with the small GTPase-Rac1 at the mitochondria. We also discuss some of the plausible mechanism(s) which allows Bcl-2 to sense and respond to the fluctuations in mitoROS.
Insights
Mitochondrial reactive oxygen species (ROS) are vital signaling molecules at low levels. The onco-protein Bcl-2 helps regulate these levels, maintaining cell homeostasis and survival.
Area of Science:
- Cell Biology
- Biochemistry
- Redox Biology
Background:
- Mitochondria are primary sources of intracellular reactive oxygen species (ROS).
- While high ROS levels cause cell damage, physiological levels act as crucial signaling molecules.
- Maintaining balanced mitochondrial ROS (mitoROS) is essential for cell homeostasis, survival, and proliferation.
Purpose of the Study:
- To review mechanisms regulating mitoROS levels.
- To highlight the role of the onco-protein Bcl-2 in redox regulation.
- To explore how Bcl-2 senses and responds to mitoROS fluctuations.
Main Methods:
- Literature review focusing on mitoROS regulation.
- Analysis of Bcl-2's involvement in mitochondrial function.
- Discussion of Bcl-2's interactions with mitochondrial components and signaling pathways.
Main Results:
- Bcl-2 regulates mitoROS through effects on mitochondrial complex IV activity.
- Bcl-2 facilitates glutathione (GSH) incorporation into mitochondria.
- Bcl-2 interacts with the small GTPase-Rac1 at the mitochondria, influencing redox signaling.
Conclusions:
- Bcl-2 plays a significant role in maintaining cellular redox balance beyond its anti-apoptotic function.
- Understanding Bcl-2's mitoROS regulatory mechanisms is key to comprehending cell homeostasis.
- Further research into Bcl-2's redox-sensing capabilities could reveal novel therapeutic targets.
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