Protective role of vitamin D against oxidative stress in diabetic retinopathy.
Maria Stella ValleCristina RussoLucia MalaguarneraPublished in: Diabetes/metabolism research and reviews (2021)
Diabetic retinopathy (DR) is a microvascular complication of diabetes mellitus. There is much evidence showing that a high level of mitochondrial overproduction of reactive oxygen species in the diabetic retina contributes in modifying cellular signalling and leads to retinal cell damage and finally to the development of DR pathogenesis. In the last few decades, it has been reported that vitamin D is involved in DR pathogenesis. Vitamin D, traditionally known as an essential nutrient crucial in bone metabolism, has also been proven to be a very effective antioxidant. It has been demonstrated that it modulates the production of advanced glycosylated end products, as well as several pathways including protein kinase C, the polyol pathway leading to the reduction of free radical formation. It prevents the translocation of nuclear factor kappa B, preventing the inflammatory response, acting as an immunomodulator, and modulates autophagy and apoptosis. In this review, we explore the molecular mechanisms by which vitamin D protects the eye from oxidative stress, in order to evaluate whether vitamin D supplementation may be useful to mitigate the deleterious effects of free radicals in DR.
Keyphrases
- diabetic retinopathy
- oxidative stress
- nuclear factor
- optical coherence tomography
- editorial comment
- inflammatory response
- toll like receptor
- diabetic rats
- dna damage
- reactive oxygen species
- ischemia reperfusion injury
- induced apoptosis
- protein kinase
- cell death
- endoplasmic reticulum stress
- type diabetes
- single cell
- cell therapy
- lipopolysaccharide induced
- heat shock
- adipose tissue
- bone mineral density
- cell cycle arrest
- skeletal muscle
- cell proliferation
- body composition
- optic nerve
- insulin resistance