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Silencing of PFKFB3 protects podocytes against high glucose ‑induced injury by inducing autophagy
In conclusion, silencing of PFKFB3 may protect podocytes from HG‑induced injury by inducing autophagy. Therefore, PFKFB3 may serve as a potential target for treatment of DN.PMID:34490476 | DOI:10.3892/mmr.2021.12405
Source: Molecular Medicine Reports - September 7, 2021 Category: Molecular Biology Authors: Zhengming Zhu Qingsheng Liu Jianshi Sun Ziyang Bao Weiwei Wang Source Type: research

Tripterygium glycoside suppresses epithelial ‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway
Mol Med Rep. 2021 Aug;24(2):592. doi: 10.3892/mmr.2021.12231. Epub 2021 Jun 24.ABSTRACTTripterygium glycoside (TG) is a traditional Chinese medicine extract with immunosuppressive, anti‑inflammatory and anti‑renal fibrosis effects. Epithelial‑mesenchymal transition (EMT) and cell apoptosis are considered to be the major cause of podocyte injury in diabetic kidney disease (DKD). However, it remains unknown as to whether TG is able to alleviate podocyte injury to prevent DKD progression. Therefore, the present study aimed to clarify the podocyte protective effects of TG on DKD. TG, Twist1 small interfering RNA (siRNA) ...
Source: Molecular Medicine Reports - June 24, 2021 Category: Molecular Biology Authors: Mei Tao Danna Zheng Xudong Liang Diandian Wu Kang Hu Juan Jin Qiang He Source Type: research

Exogenous sodium hydrosulfide protects against high glucose ‑induced injury and inflammation in human umbilical vein endothelial cells by inhibiting necroptosis via the p38 MAPK signaling pathway.
In conclusion, the findings of the present study indicated that NaHS may protect HUVECs against HG‑induced injury and inflammation by inhibiting necroptosis via the p38 MAPK signaling pathway, which may represent a promising drug for the therapy of diabetic vascular complications. PMID: 33215220 [PubMed - in process]
Source: Molecular Medicine Reports - November 21, 2020 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Cortex Mori Radicis extract promotes neurite outgrowth in diabetic rats by activating PI3K/AKT signaling and inhibiting Ca2+ influx associated with the upregulation of transient receptor potential canonical channel 1.
Authors: Lu M, Yi T, Xiong Y, Wang Q, Yin N Abstract Cortex Mori Radicis extract (CMR) has various pharmacological properties, such as anti‑inflammatory, anti‑allergic and anti‑hyperglycemic effects. However, the effects and mechanisms of CMR in the neuroregeneration of diabetic peripheral neuropathy (DPN) are unclear. In the present study, the effects of CMR on neurite outgrowth of dorsal root ganglia (DRG) neurons in diabetic rats were investigated and its underlying mechanisms were explored. SD rats were subjected to a high‑fat diet with low‑dose streptozotocin to induce a Type II diabetes model with p...
Source: Molecular Medicine Reports - January 16, 2020 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Sam68 mediates high glucose ‑induced podocyte apoptosis through modulation of Bax/Bcl‑2.
This study sought to examine the effect of Sam68 on high glucose (HG)‑induced podocytes apoptosis, and the mechanism underlying this effect. Immortalized mouse podocytes were exposed to medium containing normal glucose, or HG and Sam68 siRNA, respectively. The expression of Sam68 in podocytes was determined by fluorescence quantitative PCR (qPCR), immunofluorescence and immunoblotting. The role of Sam68 in HG‑induced podocyte apoptosis was further evaluated by inhibiting Sam68 expression by Sam68 siRNA and performing flow cytometry. The mRNA and protein expression of pro‑apoptosis gene Bax and anti‑apoptotic gene B...
Source: Molecular Medicine Reports - September 7, 2019 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Lentiviral ‑mediated Shh reverses the adverse effects of high glucose on osteoblast function and promotes bone formation via Sonic hedgehog signaling.
Lentiviral‑mediated Shh reverses the adverse effects of high glucose on osteoblast function and promotes bone formation via Sonic hedgehog signaling. Mol Med Rep. 2019 Jul 31;: Authors: Jiang ZL, Jin H, Liu ZS, Liu MY, Cao XF, Jiang YY, Bai HD, Zhang B, Li Y Abstract Patients with diabetes tend to have an increased incidence of osteoporosis, which may be associated with hyperglycemia; however, the pathogenic mechanisms governing this interaction remain unknown. The present study sought to investigate whether elevated extracellular glucose levels of bone mesenchymal stem cells (BMSCs) could influence ...
Source: Molecular Medicine Reports - August 22, 2019 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Activation of the Notch ‑Nox4‑reactive oxygen species signaling pathway induces cell death in high glucose‑treated human retinal endothelial cells.
Activation of the Notch‑Nox4‑reactive oxygen species signaling pathway induces cell death in high glucose‑treated human retinal endothelial cells. Mol Med Rep. 2018 Nov 09;: Authors: Jiao W, Ji J, Li F, Guo J, Zheng Y, Li S, Xu W Abstract Diabetic retinopathy (DR) occurs in almost all patients with diabetes and remains as one of the major causes of vision loss worldwide. Nevertheless, the molecular mechanisms underlying the pathogenesis of DR remain elusive. The present study aimed to investigate the role and association of Notch signaling and NADPH oxidase 4 (Nox4)‑mediated oxidative stress in...
Source: Molecular Medicine Reports - November 16, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Spleen tyrosine kinase promotes NLR family pyrin domain containing 3 inflammasome ‑mediated IL‑1β secretion via c‑Jun N‑terminal kinase activation and cell apoptosis during diabetic nephropathy.
Spleen tyrosine kinase promotes NLR family pyrin domain containing 3 inflammasome‑mediated IL‑1β secretion via c‑Jun N‑terminal kinase activation and cell apoptosis during diabetic nephropathy. Mol Med Rep. 2018 Jun 14;: Authors: Qiao Y, Tian X, Men L, Li S, Chen Y, Xue M, Hu Y, Zhou P, Long G, Shi Y, Liu R, Liu Y, Qi Z, Cui Y, Shen Y Abstract Diabetic nephropathy (DN) is a serious complication of diabetes and can cause an increased mortality risk. It was previously reported that NLR family pyrin domain containing 3 (NLRP3) inflammasome is involved in the pathogenesis of diabetes. However, the...
Source: Molecular Medicine Reports - June 15, 2018 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Nogo receptor knockdown and ciliary neurotrophic factor attenuate diabetic retinopathy in streptozotocin-induced diabetic rats.
Authors: Guo X, Liu X Abstract Diabetic retinopathy (DR) is a common complication of diabetes mellitus (DM). We investigated whether Nogo receptor (NgR) knockdown and ciliary neurotrophic factor (CNTF) treatment, either alone or in combination, ameliorated diabetic retinopathy (DR) in diabetic rat model. STZ‑induced diabetic rats were administrated for a total of 12 weeks with 3 µM siRNA (5 µl) once every 6 weeks and/or 1 µg CNTF weekly. The retinal tissues were excised. We measured cell number in ganglion cell layer (GCL) using H&E staining and cell apoptosis using TUNEL assay. Bax, Bcl‑2, Caspaseâ...
Source: Molecular Medicine Reports - June 29, 2017 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Lentivirus ‑mediated overexpression of CD97/ADGRE5 reverses dysregulated high glucose‑induced endothelial cell migration.
In conclusion, the present study established that the overexpression of CD97 improved high glucose‑induced dysfunction of endothelial cell migration. These findings provide insight to assist in identifying therapeutic targets with potential to ameliorate certain vascular complications of diabetes. PMID: 28358422 [PubMed - as supplied by publisher]
Source: Molecular Medicine Reports - March 31, 2017 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

High glucose-induced fibronectin upregulation in cultured mesangial cells involves caveolin-1-dependent RhoA-GTP activation via Src kinase.
In conclusion, HG‑induced FN upregulation requires caveolae and caveolin‑1 to interact with RhoA and Src kinases. Interference with Src/caveolin-1/RhoA signaling may provide novel mechanistic targets for the treatment of DKD. PMID: 27220778 [PubMed - as supplied by publisher]
Source: Molecular Medicine Reports - May 27, 2016 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

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