Table 3.

Summary of recently published studies on effects of HG or diabetes on connexins

Connexin	Cell/tissue	Results	References
Cx43	Airway epithelium	HG decreases Cx43, disassociates Cx43 interaction with tight junction and increases permeabilityof airway epithelial cells.	(Yu et al., 2016)
Cx43	Pericytes and endothelial cell (EC)	Diabetic pericytes are unable to sustain EC growth arrest in coculture and reduce Cx43.	(Durham et al., 2015)
Cx43	Foot	Cx43 mimetic peptide ACT1 accelerates the healing of chronic diabetic foot ulcers in patients.	(Grek et al., 2015)
Cx43	Vascular endothelial cell(VSMC)	Diabetes and hyperlipidemia-induced inflammatory response upregulate the expression of Cx43 through selective downregulation of miRNAs.	(Li et al., 2015)
Cx43	Endothelia cells	Cx43 expression is independent of shear stress and is upregulated by irreversibly glycated advanced glycation end-products (AGE).	(Maria et al., 2014)
Cx43 and Cx40	Heart of type 1 diabetes (T1D) rats treated with streptozotocin (STZ)	Cx43 expression increases, distribution changes and tyrosine phosphorylation decreases in STZ-induced diabetic rats; Cx40 has no change.	(Joshi et al., 2015)
Cx43	Cornea	Alpha-carboxy terminus 1 (αCT1) peptide modified from part of C-terminus suppresses inflammatory response and increases wound healing rate of corneal wound closure in STZ type-I diabetes rat model.	(Moore et al., 2014)
Cx43	Glomeruli of diabetic nephropathy and glomerular mesangial cells (GMCs)	HG decreases Cx43 and p-AMPK; Activating AMPK prevents the downregulation of Cx43 through the inhibition of mTOR. A dominant-negative AMPK reduces Cx43 expression and induces GMC senescence.	(Guo et al., 2014)
Cx43	Heart	STZ-diabetic rats benefit from n-3 polyunsaturated fatty acids (PUFA) intake likely through increased Cx43 protein (not mRNA) level by attenuating myocardial Cx43 abnormalities and improving cardiac function.	(Anna et al., 2014)
Cx43	Human corpus cavernosum (HCC) tissue	The number of Cx43 plaques is reduced in HCC tissues from diabetic or hypogonadal subjects, which may contribute to diminished erectile physiology.	(Traish et al., 2013)
Cx43	Germ cells	Gene expression of Cx43 is significantly reduced in germ cells from diabetic rats along with cell adhesion molecules.	(Aktug et al., 2013)
Cx32, Cx26 and Cx43	Sciatic nerves	COMP-Ang-1 reduces blood glucose and cholesterol in ob/ob mice and improves expression of Cx32 and Cx26, but suppress TNFα and Cx43.	(Kosacka et al., 2012)
Cx43	Human dermal fibroblasts and keratinocytes	Cx mimetic peptide Gap27 regulates extracellular matrix gene expression and improves cell migration in hyperglycemia/hyperinsulinemia, but has less influence in diabetic cells.	(Wright et al., 2012)
Cx26, 30.3, 31 and 43	Wound mouse skin	mRNAs of these four Cx subtypes are elevated in diabetic wounds and selenium downregulates Cx expression, and improves angiogenesis and wound healing.	(Bajpai et al., 2011)
Cx37, Cx40 and Cx43	Rat renal tissue	Cx43 phosphorylation is enhanced in Zucker diabetic fatty (ZDF); Cx43 Gap27 peptide impairs renal autoregulation in Zucker lean (ZL) rate, but not in ZDF rat model of type 2 diabetes.	(Takenaka et al., 2011)
Cx43	Retinal endothelial cells	HG increased matrix metalloproteinase-2 (MMP2) and decreases Cx43 in mitochondria. Overexpression of MnSOD protects retinal mitochondriaby decreasing MMP2 and increasing HSp60 and Cx43.	(Mohammad and Kowluru, 2011)
Cx43	Rat renal tissue	The increase of Cx43 in renal tissue of diabetic rat is alleviated by argirein compound along with reduction of NADPH oxidase and ER stress.	(Hu et al., 2011)