1α,25-Dihydroxyvitamin D3 promotes angiogenesis by alleviating AGEs-induced autophagy

Yu, Xiong; Zhou, Feng; Liu, Yeyu; Yi, Zumu; Wang, Xinyu; Wu, Yingying; Gong, Ping

doi:10.1016/j.abb.2021.109041

Cited by 10 publications

(5 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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%

The role of oxidative stress in diabetes mellitus-induced vascular endothelial dysfunction

An,

Xu,

Wan

et al. 2023

Cardiovasc Diabetol

View full text Add to dashboard Cite

Diabetes mellitus is a metabolic disease characterized by long-term hyperglycaemia, which leads to microangiopathy and macroangiopathy and ultimately increases the mortality of diabetic patients. Endothelial dysfunction, which has been recognized as a key factor in the pathogenesis of diabetic microangiopathy and macroangiopathy, is characterized by a reduction in NO bioavailability. Oxidative stress, which is the main pathogenic factor in diabetes, is one of the major triggers of endothelial dysfunction through the reduction in NO. In this review, we summarize the four sources of ROS in the diabetic vasculature and the underlying molecular mechanisms by which the pathogenic factors hyperglycaemia, hyperlipidaemia, adipokines and insulin resistance induce oxidative stress in endothelial cells in the context of diabetes. In addition, we discuss oxidative stress-targeted interventions, including hypoglycaemic drugs, antioxidants and lifestyle interventions, and their effects on diabetes-induced endothelial dysfunction. In summary, our review provides comprehensive insight into the roles of oxidative stress in diabetes-induced endothelial dysfunction.

show abstract

Section: Effect Of Targeting Oxidative Stress In Diabetes-induced End...mentioning

confidence: 99%

The role of oxidative stress in diabetes mellitus-induced vascular endothelial dysfunction

An,

Xu,

Wan

et al. 2023

Cardiovasc Diabetol

View full text Add to dashboard Cite

show abstract

“…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%

Level of 25-hydroxyvitamin D and vitamin D receptor in diabetic foot ulcer and factor associated with diabetic foot ulcers

Tang

Huang

Luo

et al. 2023

Diabetol Metab Syndr

View full text Add to dashboard Cite

Background At present, there is no clinical study to elucidate the correlation between vitamin D deficiency and the incidence of diabetic foot osteomyelitis (DFO).This study aims to clarify levels of 25-hydroxyvitamin D [25(OH)VD] in peripheral blood and vitamin D receptor (VDR) expression in wound margin tissues (T-VDR) of patients with type 2 diabetes mellitus (T2DM) with diabetic foot ulcer (DFU) and DFO, and to determine its correlation with treatment outcomes of DFU and DFO, and and its value as a potential biomarker for the diagnosis of DFU and DFO. Methods 156 T2DM patients with DFU (DFU group), 100 T2DM patients without DFU (T2DM group), and 100 healthy controls (NC group). The DFU group patients were subdivided into DFO (n = 80) and NDFO groups (n = 76). The level of serum 25(OH)VD was measured via chemiluminescence immunoassay, and T-VDR expression level was determined by quantitative real-time PCR. Results The levels of serum 25(OH)VD in the DFU group were significantly lower than the T2DM group [(10.3 (5.8, 18.7) vs 15.7 (8.6, 24.6) ng/mL, P = 0.002)]. Similarly, the levels of serum 25(OH)VD and T-VDR expression in the DFO group were statistically lower than the NDFO group [9.2 (5.2, 20.5) vs 12.8 (6.9, 22.1) ng/mL, P = 0.006)], [1.96 (0.61, 3.97) vs 3.11 (1.36, 5.11), P = 0.004)], respectively. Furthermore, the levels of serum 25(OH)VD and T-VDR expression in DFU patients were positively correlated with the ulcer healing rate of foot ulcer after 8 weeks of treatment ( P = 0.031, P = 0.016, respectively). Multivariate logistic regression analysis showed that low level of serum 25(OH)VD was an independent risk factor for DFU and DFO (ORDFU = 2.42, ORDFO = 3.05, P = 0.008, 0.001, respectively), and decreased T-VDR expression level was an independent risk factor for DFO (OR = 2.83, P = 0.004). Meanwhile, the ROC curve analysis indicated that the AUC of serum 25(OH)VD level for the diagnosis of DFU and DFO was 0.821 (95% CI, 0.754–0.886, P < 0.001) and 0.786 (95%CI, 0.643–0.867, P < 0.001), respectively. When establishing a diagnosis of DFO, the AUC of T-VDR expression level was 0.703 (95%CI: 0.618–0.853, P < 0.001). Conclusions The levels of serum 25(OH)VD and T-VDR expression in DFU and DFO decreased. Serum 25(OH)VD and T-VDR are potentially valuable biomarkers for diagnosis and prognosis of DFU and DFO. .

show abstract

“…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%

Calcitriol modifies tight junctions, improves barrier function, and reduces TNF‐α‐induced barrier leak in the human lung‐derived epithelial cell culture model, 16HBE 14o‐

Rybakovsky

DiGuilio

Valenzano

et al. 2023

Physiological Reports

View full text Add to dashboard Cite

Using the 16HBE 14o-human airway epithelial cell culture model, calcitriol (Vitamin D) was shown to improve barrier function by two independent metrics -increased transepithelial electrical resistance (TER) and reduced transepithelial diffusion of 14 C-D-mannitol (J m ). Both effects were concentration dependent and active out to 168 h post-treatment. Barrier improvement associated with changes in the abundance of specific tight junctional (TJ) proteins in detergent-soluble fractions, most notably decreased claudin-2. TNF-αinduced compromise of barrier function could be attenuated by calcitriol with a concentration dependence similar to that observed for improvement of control barrier function. TNFαinduced increases in claudin-2 were partially reversed by calcitriol. The ERK 1,2 inhibitor, U0126, itself improved 16HBE barrier function indicating MAPK pathway regulation of 16HBE barrier function. Calcitriol's action was additive to the effect of U0126 in reducing TNF-α -induced barrier compromise, suggesting that calcitriol may be acting through a non-ERK pathway in its blunting of TNF-α -induced barrier compromise. This was supported by calcitriol being without effect on pERK levels elevated by the action of TNF-α. Lack of effect of TNF-α on the death marker, caspase-3, and the inability of calcitriol to decrease the elevated LC3B II level caused by TNF-α, suggest that calcitriol's barrier improvement does not involve a cell death pathway. Calcitriol's improvement of control barrier function was not additive to barrier improvement induced by retinoic acid (Vitamin A). Calcitriol improvement and protection of airway barrier function could in part explain Vitamin D's reported clinical efficacy in COVID-19 and other airway diseases.

show abstract

1α,25-Dihydroxyvitamin D3 promotes angiogenesis by alleviating AGEs-induced autophagy

Cited by 10 publications

References 64 publications

The role of oxidative stress in diabetes mellitus-induced vascular endothelial dysfunction

The role of oxidative stress in diabetes mellitus-induced vascular endothelial dysfunction

Level of 25-hydroxyvitamin D and vitamin D receptor in diabetic foot ulcer and factor associated with diabetic foot ulcers

Calcitriol modifies tight junctions, improves barrier function, and reduces TNF‐α‐induced barrier leak in the human lung‐derived epithelial cell culture model, 16HBE 14o‐

Contact Info

Product

Resources

About