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Specialty: Molecular Biology
Condition: Diabetes

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Total 188 results found since Jan 2013.

Downregulation of Connexin 43 promotes vascular cell loss and excess permeability associated with the development of vascular lesions in the diabetic retina.
CONCLUSIONS: Results indicate that downregulation of Cx43 expression alone induces vascular cell death and promotes vascular permeability in the retina. These findings suggest that diabetes-induced downregulation of Cx43 participates in promoting retinal vascular lesions associated with diabetic retinopathy (DR). PMID: 24940027 [PubMed - indexed for MEDLINE]
Source: Molecular Vision - November 16, 2014 Category: Molecular Biology Tags: Mol Vis Source Type: research

Leading RNA Interference Therapeutics Part 1: Silencing Hereditary Transthyretin Amyloidosis, with a Focus on Patisiran
AbstractIn 2018, patisiran was the first-ever RNA interference (RNAi)-based drug approved by the US Food and Drug Administration. Now pharmacology textbooks may include a new drug class that  results in the effect first described by Fire and Mello 2 decades ago: post-transcriptional gene silencing by a small-interfering RNA (siRNA). Patients with hereditary transthyretin-mediated amyloidosis (hATTR amyloidosis) present with mutations in the transthyretin (TTR) gene that lead to the formation of amyloid deposits in peripheral nerves and heart. The disease may also affect the eye and central nervous system. The formulatio...
Source: Molecular Diagnosis and Therapy - November 6, 2019 Category: Molecular Biology Source Type: research

ATF5 regulates tubulointerstitial injury in diabetic kidney disease via mitochondrial unfolded protein response
CONCLUSIONS: ATF5 could exert a protective effect in a very early stage but promoted tubulointerstitial injury by regulating HSP60 and the UPRmt pathway under DKD conditions, providing a potential target for the prevention of DKD progression.PMID:37095454 | DOI:10.1186/s10020-023-00651-4
Source: Molecular Medicine - April 24, 2023 Category: Molecular Biology Authors: Yifei Liu Lei Zhang Shumin Zhang Jialu Liu Xiaohui Li Kexin Yang Danyi Yang Yu Liu Lin Sun Fuyou Liu Li Xiao Source Type: research

The augmentation of O-GlcNAcylation reduces glyoxal-induced cell injury by attenuating oxidative stress in human retinal microvascular endothelial cells.
Abstract It has recently been reported that O-linked β-N-acetyl glucosamine (O-GlcNAc) modification (a simple intracellular serine (Ser)/threonine (Thr)-linked monosaccharide) in human retinal microvascular endothelial cells (HRECs) is related to diabetic retinopathy (DR). During O-GlcNAcylation, O-GlcNAc is added to Ser and Thr residues. As the generation of reactive oxygen species (ROS) is one of the characteristics of advanced glycation end product (AGE) injury, and the most important key pathogenic factor of DR, in the present study, we aimed to investigate the association between O-GlcNAcylation and RO...
Source: International Journal of Molecular Medicine - August 20, 2015 Category: Molecular Biology Authors: Liu GD, Xu C, Feng L, Wang F Tags: Int J Mol Med Source Type: research

Overexpressing STAMP2 attenuates adipose tissue angiogenesis and insulin resistance in diabetic ApoE −/−/LDLR−/− mouse via a PPARγ/CD36 pathway
Abstract The aim of this study was to investigate whether overexpression of STAMP2 improves insulin resistance by regulating angiogenesis in adipose tissues. The characteristics of diabetic mice were measured by serial metabolite and pathology tests. Samples were obtained from epididymal, subcutaneous and brown adipose tissues. Histological and morphological analysis demonstrated that STAMP2 gene overexpression reduced adipocyte size, angiogenesis in epididymal and brown adipose tissues. On aortic ring assay, microvessels sprouting from aortas were significantly inhibited after STAMP2 gene overexpression. The cellular effe...
Source: Journal of Cellular and Molecular Medicine - June 19, 2017 Category: Molecular Biology Authors: Feng Wang, Lu Han, Ran ‐ran Qin, Yao‐yuan Zhang, Di Wang, Zhi‐Hao Wang, Meng‐Xiong Tang, Yun Zhang, Ming Zhong, Wei Zhang Tags: Original Article Source Type: research

Overexpressing STAMP2 attenuates adipose tissue angiogenesis and insulin resistance in diabetic ApoE(-/-) /LDLR(-/-) mouse via a PPAR γ/CD36 pathway.
Overexpressing STAMP2 attenuates adipose tissue angiogenesis and insulin resistance in diabetic ApoE(-/-) /LDLR(-/-) mouse via a PPARγ/CD36 pathway. J Cell Mol Med. 2017 Jun 19;: Authors: Wang F, Han L, Qin RR, Zhang YY, Wang D, Wang ZH, Tang MX, Zhang Y, Zhong M, Zhang W Abstract The aim of this study was to investigate whether overexpression of STAMP2 improves insulin resistance by regulating angiogenesis in adipose tissues. The characteristics of diabetic mice were measured by serial metabolite and pathology tests. Samples were obtained from epididymal, subcutaneous and brown adipose tissues. Hist...
Source: J Cell Mol Med - June 19, 2017 Category: Molecular Biology Authors: Wang F, Han L, Qin RR, Zhang YY, Wang D, Wang ZH, Tang MX, Zhang Y, Zhong M, Zhang W Tags: J Cell Mol Med Source Type: research

Slit2/Robo1 signaling is involved in angiogenesis of glomerular endothelial cells exposed to a diabetic-like environment
AbstractAbnormal angiogenesis plays a pathological role in diabetic nephropathy (DN), contributing to glomerular hypertrophy and microalbuminuria. Slit2/Robo1 signaling participates in angiogenesis in some pathological contexts, but whether it is involved in glomerular abnormal angiogenesis of early DN is unclear. The present study evaluated the effects of Slit2/Robo1 signaling pathway on angiogenesis of human renal glomerular endothelial cells (HRGECs) exposed to a diabetic-like environment or recombinant Slit2-N. To remove the effect of Slit2 derived from mesangial cells, human renal mesangial cells (HRMCs) grown in high...
Source: Angiogenesis - January 3, 2018 Category: Molecular Biology Source Type: research

LncRNA uc.48+ is involved in the diabetic immune and inflammatory responses mediated by P2X7 receptor in RAW264.7 macrophages.
Abstract High glucose combined with high FFAs can contribute to the unfavorable development of type 2 diabetes mellitus (T2DM) and monocytes/macrophages are important in the occurrence and development of T2DM, which is regarded as a type of low‑grade inflammation. Although our previous study demonstrated that increased expression of P2X7 receptor (P2X7R) in peripheral blood monocytes may alter the innate immune system and that long non‑coding (lnc)RNA uc.48+ was involved in diabetic neuropathic pain, the involvement of uc.48+ mediated by the P2X7R in monocyte/macrophages during T2DM has not been reported. In t...
Source: International Journal of Molecular Medicine - May 9, 2018 Category: Molecular Biology Authors: Wu H, Wen F, Jiang M, Liu Q, Nie Y Tags: Int J Mol Med Source Type: research

Effect of celastrol on toll ‑like receptor 4‑mediated inflammatory response in free fatty acid‑induced HepG2 cells.
Effect of celastrol on toll‑like receptor 4‑mediated inflammatory response in free fatty acid‑induced HepG2 cells. Int J Mol Med. 2018 Jul 12;: Authors: Han LP, Sun B, Li CJ, Xie Y, Chen LM Abstract Toll‑like receptor 4 (TLR4)‑mediated immune and inflammatory signaling serves a pivotal role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Our previous study demonstrated that celastrol treatment was able to improve hepatic steatosis and inhibit the TLR4 signaling cascade pathway in type 2 diabetic rats. The present study aimed to investigate the effects of celastrol on trigly...
Source: International Journal of Molecular Medicine - July 12, 2018 Category: Molecular Biology Authors: Han LP, Sun B, Li CJ, Xie Y, Chen LM Tags: Int J Mol Med Source Type: research

LAZ3 protects cardiac remodeling in diabetic cardiomyopathy via regulating miR-21/PPARa signaling
In conclusion, LAZ3 protects against cardiac remodeling in DCM by decreasing miR-21, thus regulating PPARa/NRF2 signaling.
Source: Biochimica et Biophysica Acta (BBA) Molecular Basis of Disease - July 19, 2018 Category: Molecular Biology Source Type: research

The differentiation of human MSCs derived from adipose and amniotic tissues into insulin-producing cells, induced by PEI@Fe3O4 nanoparticles-mediated NRSF and SHH silencing.
Abstract Type 1 diabetes involves the immunologically mediated destruction of insulin‑producing cells (IPCs) in the pancreatic islet. Mesenchymal stem cells (MSCs) have the ability to differentiate into IPCs and have become the most promising means for diabetes therapy. The present study demonstrated that human adipose‑derived stem cells (hADSCs) and human amniotic MSCs (hAMSCs) are able to differentiate into functional IPCs by knocking down neuronal restrictive silencing factor (NRSF) and Sonic hedgehog (SHH). In the current study, PEI@Fe3O4 nanoparticles (NPs) were used to deliver NRSF small interfering (si)...
Source: International Journal of Molecular Medicine - August 14, 2018 Category: Molecular Biology Authors: Wang R, Zhang D, Zhang T, Zhao F, Lang H, Lin X, Pang X Tags: Int J Mol Med 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

Inhibition of P53/miR-34a improves diabetic endothelial dysfunction via activation of SIRT1.
Abstract Endothelial dysfunction contributes to diabetic macrovascular complications, resulting in high mortality. Recent findings demonstrate a pathogenic role of P53 in endothelial dysfunction, encouraging the investigation of the effect of P53 inhibition on diabetic endothelial dysfunction. Thus, high glucose (HG)-treated endothelial cells (ECs) were subjected to pifithrin-α (PFT-α)-a specific inhibitor of P53, or P53-small interfering RNA (siRNA), both of which attenuated the HG-induced endothelial inflammation and oxidative stress. Moreover, inhibition of P53 by PFT-α or P53-siRNA prohibited P53 acetylatio...
Source: J Cell Mol Med - February 22, 2019 Category: Molecular Biology Authors: Wu J, Liang W, Tian Y, Ma F, Huang W, Jia Y, Jiang Z, Wu H Tags: J Cell Mol Med 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

H19 inhibition increases HDAC6 and regulates IRS1 levels and insulin signaling in the skeletal muscle during diabetes
CONCLUSIONS: Our results suggest a critical role for the lncRNA H19-HDAC6 axis in regulating IRS1 levels in the skeletal muscle during diabetes and therefore restoring normal H19 levels might hold a therapeutic potential for the management of aberrant skeletal muscle physiology during insulin resistance and type 2 diabetes.PMID:35842608 | DOI:10.1186/s10020-022-00507-3
Source: Molecular Medicine - July 16, 2022 Category: Molecular Biology Authors: Amit Kumar Malabika Datta Source Type: research