Hyperglycemia is a highly dangerous factor to various diseases, even resulting in death of people. Inflammation plays a key role in this process. The aim of this study was to explore the role of malignant fibrous histiocytoma amplified sequence 1 (MFHAS1) in high-glucose induced inflammation. Our research showed that high glucose stimulated the expression of MFHAS1, and overexpression of MFHAS1 can attenuate high-glucose induced inflammation in endothelial cells by decreasing the secretion of cytokines interleukin-1β (IL-1β), interleukin-1α (IL-1α), adhesion molecule intercellular adhesion molecule-1 (ICAM), interleukin-6 (IL-6), interleukin-8 (IL-8), and chemokine ligand 1 (CXCL-1). Furthermore, we found that MFHAS1 promoted the phosphorylation of Akt and the expression of heme oxygenase-1 (HO-1). Our results indicated that MFHAS1 deadened high-glucose induced inflammation by activating AKT/HO-1 pathway, suggesting that MFHAS1 may act as a new therapeutic target of diabetes mellitus.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10753-017-0696-0DOI Listing

Publication Analysis

Top Keywords

high-glucose induced
12
induced inflammation
12
high glucose
8
expression mfhas1
8
akt/ho-1 pathway
8
endothelial cells
8
mfhas1
7
inflammation
5
glucose stimulates
4
stimulates expression
4

Similar Publications

PDIA4 targets IRE1α/sXBP1 to alleviate NLRP3 inflammasome activation and renal tubular injury in diabetic kidney disease.

Biochim Biophys Acta Mol Basis Dis

December 2024

Department of Pathology, School of Medicine, Nankai University, Tianjin, China. Electronic address:

The role of ER stress in the pathogenesis of diabetic kidney diseases (DKD) remains unclear. We employed bioinformatics to identify the UPR pathway activation, inflammation, and programmed cell death patterns in diabetic tubules. Levels of IRE1α/sXBP1 signaling, NLRP3 inflammasome activity and pyroptosis in tubular cells under high glucose conditions were measured.

View Article and Find Full Text PDF

The aim of this study was to evaluate for the effects of forsythiaside A (FA) on myocardial injury in streptozotocin (STZ)-induced diabetes mice. Blood glucose (BG), serum triglycerides (TG), lactate dehydrogenase (LDH), creatine kinase isoenzyme (CK-MB), cardiac troponin (cTnI), malondialdehyde (MDA), superoxide dismutase (SOD) levels were detected in STZ mice. The structure and function of heart was observed via cardiac ultrasound.

View Article and Find Full Text PDF

O-GlcNAcylation is a dynamic post-translational modification involving the attachment of N-acetylglucosamine to serine and threonine residues. This review emphasizes its role in regulating the signaling pathways of pyroptosis. Specifically, the O-GlcNAcylation of GSDMD is linked to the modulation of pyroptosis, suggesting that enhancing O-GlcNAcylation of GSDMD could be crucial for improving hypoperfusion in sepsis.

View Article and Find Full Text PDF

The aldose reductase inhibitors AT-001, AT-003 and AT-007 attenuate human keratinocyte senescence.

Front Aging

December 2024

Diabetes Research Program, Holman Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, New York University School of Medicine, New York, NY, United States.

Human skin plays an important role protecting the body from both extrinsic and intrinsic factors. Skin aging at cellular level, which is a consequence of accumulation of irreparable senescent keratinocytes is associated with chronological aging. However, cell senescence may occur independent of chronological aging and it may be accelerated by various pathological conditions.

View Article and Find Full Text PDF

Aim: Imbalanced M1/M2 macrophage phenotype activation is a key point in diabetic kidney disease (DKD). Macrophages mainly exhibit the M1 phenotype, which contributes to inflammation and fibrosis in DKD. Studies have indicated that autophagy plays an important role in M1/M2 activation.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!