The Role of MicroRNAs in Diabetes-Related Oxidative Stress.
Mirza Muhammad Fahd QadirDagmar KleinSilvia Álvarez-CubelaJuan Domínguez-BendalaRicardo Luis PastoriPublished in: International journal of molecular sciences (2019)
Cellular stress, combined with dysfunctional, inadequate mitochondrial phosphorylation, produces an excessive amount of reactive oxygen species (ROS) and an increased level of ROS in cells, which leads to oxidation and subsequent cellular damage. Because of its cell damaging action, an association between anomalous ROS production and disease such as Type 1 (T1D) and Type 2 (T2D) diabetes, as well as their complications, has been well established. However, there is a lack of understanding about genome-driven responses to ROS-mediated cellular stress. Over the last decade, multiple studies have suggested a link between oxidative stress and microRNAs (miRNAs). The miRNAs are small non-coding RNAs that mostly suppress expression of the target gene by interaction with its 3'untranslated region (3'UTR). In this paper, we review the recent progress in the field, focusing on the association between miRNAs and oxidative stress during the progression of diabetes.
Keyphrases
- oxidative stress
- reactive oxygen species
- dna damage
- induced apoptosis
- type diabetes
- cell death
- cardiovascular disease
- glycemic control
- ischemia reperfusion injury
- diabetic rats
- cell cycle arrest
- poor prognosis
- single cell
- weight gain
- stress induced
- risk factors
- body mass index
- nitric oxide
- signaling pathway
- endoplasmic reticulum stress
- adipose tissue
- hydrogen peroxide
- mesenchymal stem cells
- metabolic syndrome
- protein kinase
- gene expression
- long non coding rna
- insulin resistance
- copy number
- physical activity