Interesting link. Really not sure what to make of it!
J Cell Physiol . 2021 Aug 25.
doi: 10.1002/jcp.30563. Online ahead of print.
Thyroid stimulating hormone aggravates diabetic retinopathy through the mitochondrial apoptotic pathway
Dong Lin 1 2 3 , Ruijie Qin 1 2 , Lixin Guo 1 2
Affiliations
• PMID: 34435365
• DOI: 10.1002/jcp.30563
Abstract
Diabetic retinopathy (DR) is a common complication of diabetes mellitus. High glucose-induced mitochondrial apoptosis is involved in the loss of retinal pericytes (PCs), which is considered to be a predominant pathologic change of diabetic retinopathy (DR). A high thyroid stimulating hormone (TSH) serum level is associated with an increased prevalence of DR in diabetic patients. Here, we investigated whether TSH regulated glucose-induced PCs loss through TSH-receptor (TSHR)-dependent mitochondrial apoptosis. First, the serum TSH level was found to be an independent risk factor for DR in Type 2 diabetic study participants (odds ratio = 2.294; 95% confidence interval: 1.925-2.733; p ≤ 0.001). Second, human PCs were treated with different concentrations of glucose, with or without bovine TSH (b-TSH). Glucose induced mitochondrial apoptosis through various mechanisms, including through regulating the expression of apoptosis-related proteins and inducing mitochondrial dysfunction, which could be deteriorated by costimulation of glucose and b-TSH. Additionally, we detected functional TSHR in PCs; blocking TSHR significantly restricted TSH-induced apoptosis. Thus, the presence of functional TSHR in human retinal PCs may facilitate the effect of high TSH on high glucose-induced PCs loss through TSHR-dependent mitochondrial apoptosis.
Keywords: apoptosis; diabetic retinopathy; mitochondria; pericytes; thyroid stimulating hormone.
Yet again, paper behind paywall: