MicroRNAs as Regulators of Radiation-Induced Oxidative Stress.
Branislav KuraPatricia PavelkovaBarbora KalocayovaMargita PobijakovaJan SlezakPublished in: Current issues in molecular biology (2024)
microRNAs (miRNAs) represent small RNA molecules involved in the regulation of gene expression. They are implicated in the regulation of diverse cellular processes ranging from cellular homeostasis to stress responses. Unintended irradiation of the cells and tissues, e.g., during medical uses, induces various pathological conditions, including oxidative stress. miRNAs may regulate the expression of transcription factors (e.g., nuclear factor erythroid 2 related factor 2 (Nrf2), nuclear factor kappa B (NF-κB), tumor suppressor protein p53) and other redox-sensitive genes (e.g., mitogen-activated protein kinase (MAPKs), sirtuins (SIRTs)), which trigger and modulate cellular redox signaling. During irradiation, miRNAs mainly act with reactive oxygen species (ROS) to regulate the cell fate. Depending on the pathway involved and the extent of oxidative stress, this may lead to cell survival or cell death. In the context of radiation-induced oxidative stress, miRNA-21 and miRNA-34a are among the best-studied miRNAs. miRNA-21 has been shown to directly target superoxide dismutase (SOD), or NF-κB, whereas miRNA-34a is a direct regulator of NADPH oxidase (NOX), SIRT1, or p53. Understanding the mechanisms underlying radiation-induced injury including the involvement of redox-responsive miRNAs may help to develop novel approaches for modulating the cellular response to radiation exposure.
Keyphrases
- nuclear factor
- radiation induced
- oxidative stress
- induced apoptosis
- toll like receptor
- reactive oxygen species
- gene expression
- cell death
- radiation therapy
- transcription factor
- dna damage
- ischemia reperfusion injury
- diabetic rats
- cell fate
- cell cycle arrest
- signaling pathway
- dna methylation
- poor prognosis
- healthcare
- hydrogen peroxide
- inflammatory response
- endoplasmic reticulum stress
- immune response
- tyrosine kinase
- pi k akt
- protein kinase
- cell proliferation
- protein protein