Role of reactive oxygen species in myelodysplastic syndromes.
Qiangan JingChaoting ZhouJunyu ZhangPing ZhangYunyi WuJunyu ZhouXiangmin TongYanchun LiJing DuYing WangPublished in: Cellular & molecular biology letters (2024)
Reactive oxygen species (ROS) serve as typical metabolic byproducts of aerobic life and play a pivotal role in redox reactions and signal transduction pathways. Contingent upon their concentration, ROS production not only initiates or stimulates tumorigenesis but also causes oxidative stress (OS) and triggers cellular apoptosis. Mounting literature supports the view that ROS are closely interwoven with the pathogenesis of a cluster of diseases, particularly those involving cell proliferation and differentiation, such as myelodysplastic syndromes (MDS) and chronic/acute myeloid leukemia (CML/AML). OS caused by excessive ROS at physiological levels is likely to affect the functions of hematopoietic stem cells, such as cell growth and self-renewal, which may contribute to defective hematopoiesis. We review herein the eminent role of ROS in the hematological niche and their profound influence on the progress of MDS. We also highlight that targeting ROS is a practical and reliable tactic for MDS therapy.
Keyphrases
- reactive oxygen species
- cell death
- acute myeloid leukemia
- dna damage
- oxidative stress
- stem cells
- cell proliferation
- systematic review
- drinking water
- bone marrow
- drug delivery
- cell cycle
- cell cycle arrest
- high intensity
- induced apoptosis
- ischemia reperfusion injury
- intellectual disability
- weight gain
- replacement therapy