Filtered By:
Condition: Diabetes Type 1

This page shows you your search results in order of date. This is page number 5.

Order by Relevance | Date

Total 127 results found since Jan 2013.

Pharmacological inhibition of MyD88 suppresses inflammation in tubular epithelial cells and prevents diabetic nephropathy in experimental mice
Acta Pharmacol Sin. 2021 Sep 22. doi: 10.1038/s41401-021-00766-6. Online ahead of print.ABSTRACTEmerging evidence shows that chronic inflammation mediated by toll-like receptors (TLRs) contributes to diabetic nephropathy. Myeloid differentiation primary-response protein-88 (MyD88) is an essential adapter protein of all TLRs except TLR3 in innate immunity. It is unclear whether MyD88 could be a therapeutic target for diabetic nephropathy. Here, we used a new small-molecule MyD88 inhibitor, LM8, to examine the pharmacological inhibition of MyD88 in protecting kidneys from inflammatory injury in diabetes. We showed that MyD88...
Source: Acta Pharmacologica Sinica - September 23, 2021 Category: Drugs & Pharmacology Authors: Qiu-Yan Zhang Su-Jing Xu Jian-Chang Qian Li-Bin Yang Peng-Qin Chen Yi Wang Xiang Hu Ya-Li Zhang Wu Luo Guang Liang Source Type: research

A Novel Resolution of Diabetes: C-C Chemokine Motif Ligand 4 Is a Common Target in Different Types of Diabetes by Protecting Pancreatic Islet Cell and Modulating Inflammation
This study aimed to investigate if CCL4 could be a potential target to improve blood sugar control in different experimental DM models. Streptozotocin-induced diabetic mice, Leprdb/JNarl diabetic mice, and C57BL/6 mice fed a high fat diet were used as the type 1 DM, type 2 DM, and metabolic syndrome model individually. Mice were randomly assigned to receive an anti-CCL4 neutralizing monoclonal antibody. The pancreatic β-cells were treated with streptozotocin for in vitro experiments. In streptozotocin-induced diabetic mice, inhibition of CCL4 controlled blood sugar, increased serum insulin levels, increased islet cell pro...
Source: Frontiers in Immunology - April 23, 2021 Category: Allergy & Immunology Source Type: research

Inhibition of PHLPP1 ameliorates cardiac dysfunction via activation of the PI3K/Akt/mTOR signalling pathway in diabetic cardiomyopathy.
CONCLUSION: Our study indicated that PHLPP1 inhibition alleviated cardiac dysfunction via activating the PI3K/Akt/mTOR signalling pathway in DCM. Therefore, PHLPP1 may be a novel therapeutic target for human DCM. PMID: 32150791 [PubMed - as supplied by publisher]
Source: J Cell Mol Med - March 8, 2020 Category: Molecular Biology Authors: Zhang M, Wang X, Liu M, Liu D, Pan J, Tian J, Jin T, Xu Y, An F Tags: J Cell Mol Med Source Type: research

Dopamine 1 receptor activation protects mouse diabetic podocytes injury via regulating the PKA/NOX-5/p38  MAPK axis.
In conclusion, D1R activation can protect diabetic podocytes from apoptosis and oxidative damage, in part through the PKA/NOX-5/p38 MAPK pathway. PMID: 31954110 [PubMed - as supplied by publisher]
Source: Experimental Cell Research - January 14, 2020 Category: Cytology Authors: Shao X, Zhang X, Hu J, Gao T, Chen J, Xu C, Wei C Tags: Exp Cell Res Source Type: research

Allopurinol reduces oxidative stress and activates Nrf2/p62 to attenuate diabetic cardiomyopathy in rats.
Abstract Allopurinol (ALP) attenuates oxidative stress and diabetic cardiomyopathy (DCM), but the mechanism is unclear. Activation of nuclear factor erythroid 2-related factor 2 (Nrf2) following the disassociation with its repressor Keap1 under oxidative stress can maintain inner redox homeostasis and attenuate DCM with concomitant attenuation of autophagy. We postulated that ALP treatment may activate Nrf2 to mitigate autophagy over-activation and consequently attenuate DCM. Streptozotocin-induced type 1 diabetic rats were untreated or treated with ALP (100 mg/kg/d) for 4 weeks and terminated after heart functi...
Source: J Cell Mol Med - December 18, 2019 Category: Molecular Biology Authors: Luo J, Yan D, Li S, Liu S, Zeng F, Cheung CW, Liu H, Irwin MG, Huang H, Xia Z Tags: J Cell Mol Med Source Type: research

Hyperglycemia-induced cardiomyocyte death is mediated by lysosomal membrane injury and aberrant expression of cathepsin D.
Abstract Hyperglycemia is an independent risk factor for diabetic heart failure. However, the mechanisms that mediate hyperglycemia-induced cardiac damage remain poorly understood. Previous studies have shown an association between lysosomal dysfunction and diabetic heart injury. The present study examined if mimicking hyperglycemia in cultured cardiomyocytes could induce lysosomal membrane permeabilization (LMP), leading to the release of lysosome enzymes and subsequent cell death. High glucose (HG) reduced the number of lysosomes with acidic pH as shown by a fluorescent pH indicator. Also, HG induced lysosomal m...
Source: Biochemical and Biophysical Research communications - December 16, 2019 Category: Biochemistry Authors: Kobayashi S, Zhao F, Kobayashi T, Hagiwara M, Kaminaris A, Li C, Cai F, Huang Y, Liang Q Tags: Biochem Biophys Res Commun Source Type: research

Klotho improves diabetic cardiomyopathy by suppressing the NLRP3 inflammasome pathway
Publication date: Available online 15 August 2019Source: Life SciencesAuthor(s): Xuelian Li, Zhiyang Li, Bingong Li, Xianjie Zhu, Xingjun LaiAbstractAimsNLRP3 inflammasome activation is essential for the development and prognosis of diabetic cardiomyopathy (DCM). The anti-aging protein Klotho is suggested to modulate tissue inflammatory responses. The aim of the present study was to examine the protective effects of Klotho on DCM.Main methodsA streptozotocin-induced diabetes mouse model was established to assess the effects of Klotho in vivo, which was administered for 12 weeks. The characteristics of type 1 DCM were eva...
Source: Life Sciences - August 18, 2019 Category: Biology Source Type: research

Tangshen Formula Alleviates Hepatic Steatosis by Inducing Autophagy Through the AMPK/SIRT1 Pathway
Conclusion In conclusion, the present study demonstrated that autophagy was involved in relieving the effects of TSF against NAFLD, which were mediated by the AMPK/SIRT1 pathway (Figure 7D). These findings may improve our current understanding of the role of TSF in treating hepatic steatosis and provide an experimental basis for the clinical application of TSF in NAFLD and its related metabolic syndrome. Ethics Statement This study was carried out in accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. The protocol was approved by the Ethics Co...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research

Gene Therapy Leaves a Vicious Cycle
Reena Goswami1, Gayatri Subramanian2, Liliya Silayeva1, Isabelle Newkirk1, Deborah Doctor1, Karan Chawla2, Saurabh Chattopadhyay2, Dhyan Chandra3, Nageswararao Chilukuri1 and Venkaiah Betapudi1,4* 1Neuroscience Branch, Research Division, United States Army Medical Research Institute of Chemical Defense, Aberdeen, MD, United States 2Department of Medical Microbiology and Immunology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, United States 3Roswell Park Comprehensive Cancer Center, Buffalo, NY, United States 4Department of Physiology and Biophysics, Case Western Reserve University, Clev...
Source: Frontiers in Oncology - April 23, 2019 Category: Cancer & Oncology Source Type: research

Resveratrol Promotes Diabetic Wound Healing via SIRT1-FOXO1-c-Myc Signaling Pathway-Mediated Angiogenesis
Conclusion: Our findings indicate that the positive role of RES in diabetic wound healing via its SIRT1-dependent endothelial protection and pro-angiogenic effects involves the inhibition of FOXO1 and the de-repression of c-Myc expression. Introduction Diabetes mellitus is a metabolic disease with an increasing incidence worldwide (Zimmet et al., 2014). The disease often leads to the development of serious complications such as microangiopathy, mainly including retinopathy, nephropathy, neuropathy, and diabetic non-healing skin ulcers (Zheng et al., 2018). Diabetic non-healing skin ulcers such as foot ulcers are ca...
Source: Frontiers in Pharmacology - April 23, 2019 Category: Drugs & Pharmacology Source Type: research

TonEBP Suppresses the HO-1 Gene by Blocking Recruitment of Nrf2 to Its Promoter
Discussion Dynamic changes in the functional phenotype of macrophages are associated with pathogenesis of inflammatory diseases (5–7). TonEBP primes macrophages toward an M1 phenotype, which has pro-inflammatory properties. TonEBP does this by promoting expression of pro-inflammatory genes via interaction with NF-κB (36) and by binding directly to the promoter (37, 64). In addition, TonEBP suppresses expression of the anti-inflammatory cytokine IL-10 by limiting chromatin access to the promoter (37). The pro-inflammatory function of TonEBP suggests that inhibiting its expression or activation could suppres...
Source: Frontiers in Immunology - April 17, 2019 Category: Allergy & Immunology Source Type: research

Increasing Upstream Chromatin Long –Range Interactions May Favor Induction of Circular RNAs in LysoPC-Activated Human Aortic Endothelial Cells
We examined the sponging potential of all significantly changed circRNAs using the CircInteractome database (Montefiori et al., 2018), recording two miRNAs with four or more predicted binding sites in a single circRNA transcript, a threshold above which meaningful sponging activity is likely to occur Memczak et al. (2013). Another four significantly changed circRNAs are experimentally shown to sponge miRNAs (Dudekula et al., 2016; Chen et al., 2017; Yan et al., 2017; Wang et al., 2018), for six total circRNAs with miRNA sponging activity including miR125, miR143, miR1272, miR153, miR515-5p, and miR196a-5p (Table 4). In Fig...
Source: Frontiers in Physiology - April 17, 2019 Category: Physiology Source Type: research

Antibodies against H1N1 influenza virus hemagglutinin cross-react with prohibitin.
Abstract Influenza virus infection is associated with type 1 diabetes (T1DM), but its pathogenesis remains unclear. Here, our study found that one of the monoclonal antibodies against H1N1 influenza virus hemagglutinin(HA) cross-reacted with human pancreatic tissue and further demonstrated that it binded to rat islet β-cells. We immunoprecipitated islet protein with this cross-reactive antibody and identified the bound antigen as prohibitin by mass spectrometry. We then expressed the prohibitin protein in bacteria and confirmed the antibody binding to prohibitin by Western blot. We also verified the cross-reactiv...
Source: Biochemical and Biophysical Research communications - April 5, 2019 Category: Biochemistry Authors: Sun L, Li H, Sun J, Guo C, Feng Y, Li Y, Zhao X, Xie X, Hu J Tags: Biochem Biophys Res Commun Source Type: research

Pancreatic {beta}-cells detoxify H2O2 through the peroxiredoxin/thioredoxin antioxidant system Metabolism
Oxidative stress is thought to promote pancreatic β-cell dysfunction and contribute to both type 1 and type 2 diabetes. Reactive oxygen species (ROS), such as superoxide and hydrogen peroxide, are mediators of oxidative stress that arise largely from electron leakage during oxidative phosphorylation. Reports that β-cells express low levels of antioxidant enzymes, including catalase and GSH peroxidases, have supported a model in which β-cells are ill-equipped to detoxify ROS. This hypothesis seems at odds with the essential role of β-cells in the control of metabolic homeostasis and organismal survival through exquisite...
Source: Journal of Biological Chemistry - March 28, 2019 Category: Chemistry Authors: Jennifer S. Stancill, Katarzyna A. Broniowska, Bryndon J. Oleson, Aaron Naatz, John A. Corbett Tags: Signal Transduction Source Type: research