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

Protective Effects of Thalidomide on High-Glucose-Induced Podocyte Injury through In Vitro Modulation of Macrophage M1/M2 Differentiation.

Journal of immunology research - 1 Jan 2020

Liao Hui, Li Yuanping, Zhang Xilan, Zhao Xiaoyun, Zheng Dan, Shen Dayue, Li Rongshan

Abstract excerpt

Objective. It has been shown that podocyte injury represents an important pathological basis that contributes to proteinuria and eventually leads to kidney failure. High glucose (HG) activates macrophage polarization, further exacerbating HG-induced podocyte injury. Our previous study on diabetic nephropathy rats indicated that thalidomide (Tha) has renoprotective properties. The present study explored the...

Read the complete abstract on PubMed

Topics

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

Share to Blood Glucose
Share to Cell Plasticity

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Glucose

Share to Macrophage Activation

Share to Oxidation-Reduction

Share to Podocytes

Share to Protective Agents

Share to Thalidomide

Source

Open in PubMed Open full text

Identifiers

PMID: 32908940
DOI: 10.1155/2020/8263598
PMCID: PMC7474395

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

Protective Effects of Thalidomide on High-Glucose-Induced Podocyte Injury through In Vitro Modulation of Macrophage M1/M2 Differentiation.PMID 32908940Read ↗

Vitamin D prevents podocyte injury via regulation of macrophage M1/M2 phenotype in diabetic nephropathy rats.Semantic proximity Read ↗

Macrophage Phenotype and Fibrosis in Diabetic Nephropathy.Semantic proximity Read ↗

Mitophagy regulates macrophage phenotype in diabetic nephropathy rats.Semantic proximity Read ↗

Paeoniflorin inhibits high glucose-induced macrophage activation through TLR2-dependent signal pathways.Semantic proximity Read ↗

Mesenchymal stem cells polarize macrophages to an anti-inflammatory phenotype to ameliorate diabetic nephropathySemantic proximity Read ↗

Notch/NICD/RBP-J Signaling Axis Regulates M1 Polarization of Macrophages Mediated by Advanced Glycation End ProductsSemantic proximity Read ↗

Pro-inflammatory/Th1 gene expression shift in high glucose stimulated mesangial cells and tubular epithelial cells.Semantic proximity Read ↗

High glucose promotes macrophage switching to M1 phenotype via down-regulating STAT-3 mediated- autophagySemantic proximity Read ↗

Relationship between Macrophages and Tissue Microenvironments in Diabetic KidneysSemantic proximity Read ↗

Macrophages polarization in renal inflammation and fibrosis animal models (Review)Semantic proximity Read ↗

The phenotype and functional alterations of macrophages in mice with hyperglycemia for long term.Semantic proximity Read ↗

High glucose promotes macrophage switching to the M1 phenotype via the downregulation of STAT-3 mediated autophagy.Semantic proximity Read ↗

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