Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Oxidative stress-induced JNK activation contributes to proinflammatory phenotype of aging diabetic mesangial cells.

American journal of physiology. Renal physiology - 1 Dec 2009

Wu Jin, Mei Changlin, Vlassara Helen, Striker Gary E, Zheng Feng

Abstract excerpt

Chronic inflammation and increased oxidative stress (OS) play an important role in diabetic nephropathy progression. Herein, we show that mesangial cells from streptozotocin-induced aging diabetic mice, a model of progressive diabetic nephropathy, exhibited increased OS and a proinflammatory phenotype characterized by elevated chemokines and ICAM-1 expression. This phenotypic change was consistent with the...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cellular Senescence
Share to Chemokine CCL2

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Chemokine CXCL1

Share to Diabetes Mellitus, Experimental

Share to Dual-Specificity Phosphatases

Share to Glomerular Mesangium

Share to JNK Mitogen-Activated Protein Kinases

Share to Kidney Glomerulus

Source

Open in PubMed Open full text

Identifiers

PMID: 19776174
DOI: 10.1152/ajprenal.00078.2009
PMCID: PMC2801342

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Oxidative stress-induced JNK activation contributes to proinflammatory phenotype of aging diabetic mesangial cells.PMID 19776174Read ↗

JNK and cardiometabolic dysfunctionSemantic proximity Read ↗

Klotho attenuates renal hypertrophy and glomerular injury in Ins2Akita diabetic mice.Semantic proximity Read ↗

Aging phenotype(s) in kidneys of diabetic mice are p66ShcA dependent.Semantic proximity Read ↗

AGE-receptor-1 counteracts cellular oxidant stress induced by AGEs via negative regulation of p66shc-dependent FKHRL1 phosphorylation.Semantic proximity Read ↗

p38 MAPK and MAPK kinase 3/6 mRNA and activities are increased in early diabetic glomeruliSemantic proximity Read ↗

Inhibition of C-jun N-terminal kinase improves insulin sensitivity but worsens albuminuria in experimental diabetes.Semantic proximity Read ↗

Glycolaldehyde-derived advanced glycation end products promote macrophage proliferation via the JAK-STAT signaling pathwaySemantic proximity Read ↗

Activation of the sphingosine kinase-signaling pathway by high glucose mediates the proinflammatory phenotype of endothelial cells.Semantic proximity Read ↗

Macrophage-derived tumor necrosis factor-α mediates diabetic renal injury.Semantic proximity Read ↗

Reduction of renal superoxide dismutase in progressive diabetic nephropathy.Semantic proximity Read ↗

RhoA/ROCK-dependent moesin phosphorylation regulates AGE-induced endothelial cellular response.Semantic proximity Read ↗

Effects of eicosapentaenoic acid on the early stage of type 2 diabetic nephropathy in KKA(y)/Ta mice: involvement of anti-inflammation and antioxidative stress.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.