2021
DOI: 10.1016/j.abb.2021.109041
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1α,25-Dihydroxyvitamin D3 promotes angiogenesis by alleviating AGEs-induced autophagy

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Cited by 10 publications
(5 citation statements)
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“…Additionally, the combination of CrPic and VD3 significantly decreased the levels of homocysteine and MDA in T2DM patient blood and enhanced endothelial function [ 138 ]. The administration of 1α,25-dihydroxyvitamin D3 (a hormonal form of VD) to vascular endothelial cells cultured in vitro promoted the expression of angiogenic markers and promoted angiogenesis by inhibiting oxidative stress and excessive autophagy through AGE-RAGE interactions and the PI3K/Akt pathway [ 139 ].…”
Section: Effect Of Targeting Oxidative Stress In Diabetes-induced End...mentioning
confidence: 99%
“…Additionally, the combination of CrPic and VD3 significantly decreased the levels of homocysteine and MDA in T2DM patient blood and enhanced endothelial function [ 138 ]. The administration of 1α,25-dihydroxyvitamin D3 (a hormonal form of VD) to vascular endothelial cells cultured in vitro promoted the expression of angiogenic markers and promoted angiogenesis by inhibiting oxidative stress and excessive autophagy through AGE-RAGE interactions and the PI3K/Akt pathway [ 139 ].…”
Section: Effect Of Targeting Oxidative Stress In Diabetes-induced End...mentioning
confidence: 99%
“…Gonzalez-Curiel et al reported that 1,25(OH)2D3 can upregulate the expression of DEFB4 and CAMP genes in primary keratinocytes from DFU, increase the production of HBD-2 and LL-37 in cell-culture supernatant, and improve the migration ability and antibacterial activity of keratinocytes, thus promoting wound healing [35]. Xiong et al found that 1,25(OH)2D3 can inhibit excessive autophagy and oxidative stress in vascular endothelial cells caused by advanced glycation end products (AGEs) through the PI3K/Akt pathway, thereby promoting angiogenesis in a high-glucose environment [36], which is conducive to wound healing. Animal experiments have demonstrated that vitamin D can improve wound healing in diabetic mice by inhibiting the expression of inflammatory genes such as IL-6 and IL-1β mediated by NF-κB [37] and inhibiting endoplasmic reticulum stress [38].…”
Section: Discussionmentioning
confidence: 99%
“…At present we have however not identified this pathway by which calcitriol is countering TNF‐α ‐induced barrier compromise. Potential candidates for this non‐ERK pathway by which calcitriol could regulate barrier function could include pathways leading to cell death, as there is extensive published literature describing calcitriol‐mediated inhibition of both apoptosis and autophagy (Langberg et al, 2009 ; Lyu et al, 2020 ; Xiong et al, 2021 ). However, the lack of any significant effect of TNF‐α on caspase‐3 levels in 16HBE, and the lack of effect of calcitriol on the increase in LC3B II levels caused by TNF‐α (Figure 12 ), suggest that this unknown calcitriol pathway is not a death pathway.…”
Section: Discussionmentioning
confidence: 99%