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Glycemic variability is associated with vascular calcification by the markers of endoplasmic reticulum stress-related apoptosis, Wnt1, galectin-3 and BMP-2.

Abstract：

Background:The present study identified whether glycemic variability (GV) was associated with vascular calcification and explored the underlying mechanisms. Methods:Eighty-four consecutive type 2 diabetic patients with unstable angina (UA) were included from January 2018 to June 2018 to calculate calcification scores using computerized tomographic angiography (CTA), and the patients were divided into 2 groups: high calcification score group (HCS group) and low calcification score group (LCS group). Intergroup differences in GV were determined via comparisons of the standard deviation (SD) of blood glucose. Calcification staining, content measurement, apoptosis evaluation and Western blot analysis of endoplasmic reticulum (ER) stress-related apoptosis, Wnt1, galectin-3 and bone morphogenetic protein-2 (BMP-2) were compared in cell cultures from rat vascular smooth muscle cells in the different degrees of GV. Results:The SD increased significantly with the increases in calcification scores from human studies (HCS group 2.37 ± 0.82 vs. LCS group 1.87 ± 0.78, p = 0.007). Multivariate logistic regression analysis suggested that increased SD and serum creatinine were independent predictors of calcification. The high GV group had a higher apoptotic rate, higher calcification content and higher expressions of glucose-regulated protein, caspase-3, Wnt1, galectin-3 and BMP-2 markers compared to the low GV group in the in vitro studies (p < 0.001). Conclusion:We report the novel finding that GV is associated with vascular calcification, and ER stress-related apoptosis, Wnt1, galectin-3 and BMP-2 may be involved in this regulation.

journal_name

Diabetol Metab Syndr

journal_title

Diabetology & metabolic syndrome

authors

Zhang L,Sun H,Liu S,Gao J,Xia J

doi

10.1186/s13098-019-0464-4

subject

Has Abstract

pub_date

2019-08-19 00:00:00

pages

67

issn

1758-5996

pii

464

journal_volume

11

pub_type

杂志文章

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