Influence of Diabetes-Induced Glycation and Oxidative Stress on the Human Rotator Cuff.
Tomoya YoshikawaYutaka MifuneAtsuyuki InuiHanako NishimotoKohei YamauraShintaro MukoharaIssei ShinoharaRyosuke KurodaPublished in: Antioxidants (Basel, Switzerland) (2022)
Most shoulder rotator cuff tears (RCTs) are caused by non-traumatic age-related rotator cuff degeneration, of which hyperglycemia is a risk factor due to its glycation reaction and oxidative stress. We aimed to identify the influence of diabetes-induced glycation and oxidative stress in patients with non-traumatic shoulder RCTs. Twenty patients, aged over 50 years, with non-traumatic shoulder RCTs participated in this study. Patients with a history of diabetes mellitus or preoperative HbA1c ≥ 6.5% were assigned to the diabetic group ( n = 10), and the rest to the non-diabetic group ( n = 10). Cell proliferation; expression of genes related to oxidative stress, glycation reaction, inflammation, and collagen; intracellular reactive oxygen species (ROS) levels; and apoptosis rates were analyzed. The diabetic group had significantly lower cell proliferation than the non-diabetic group. In the diabetic group, the mRNA expression levels of NOX1 , NOX4 , IL6 , RAGE , type III collagen, MMP2 , TIMP1 , and TIMP2 were significantly higher; type I collagen expression was significantly lower; and the rate of ROS-positive cells and apoptotic cells, as well as the expression of advanced glycation end-products (AGEs) and the receptor for AGEs (RAGE), was significantly higher. In conclusion, hyperglycemia caused by diabetes mellitus increased AGE and RAGE expression, and led to increased NOX expression, ROS production, and apoptosis in the human rotator cuff. This provides scope to find a preventive treatment for non-traumatic RCTs by inhibiting glycation and oxidative stress.
Keyphrases
- rotator cuff
- oxidative stress
- diabetic rats
- reactive oxygen species
- induced apoptosis
- poor prognosis
- type diabetes
- dna damage
- wound healing
- cell death
- cell cycle arrest
- cell proliferation
- spinal cord injury
- endoplasmic reticulum stress
- ischemia reperfusion injury
- endothelial cells
- binding protein
- cardiovascular disease
- glycemic control
- end stage renal disease
- signaling pathway
- ejection fraction
- pi k akt
- gene expression
- cell cycle
- risk factors
- long non coding rna
- high glucose
- newly diagnosed
- patients undergoing
- peritoneal dialysis
- insulin resistance
- induced pluripotent stem cells
- type iii
- genome wide
- metabolic syndrome
- patient reported
- drug induced
- dna methylation
- weight loss