Targeting inflammation for the treatment of Diabetic Kidney Disease: a five-compartment mechanistic model

BMC Nephrology

Table 1 Examples of inflammatory molecular pathways in diabetic kidney disease

Damage-associated molecular patterns	HMGB1, HSPs, fibronectin Advanced glycation end-products IL-33
Pattern-recognition molecules	TLR2, TLR4 NLR RAGE MBL (complement)
Intracellular signaling	JAK/STAT, NF-kB, Nrf2 NLRP3 inflammasome
Chemokines	CCL2, CCL5, CSF1, CXCL1, CXCL16, CXCL-10, CXCL-16, IL-8
Cytokines	IL-6, TNF-α, IL-1β, IL-18, IL-17A, TGF-β1, CX3CL1
Adhesion molecules	ICAM-1, VCAM-1, Galectin-3, Integrin αVβ3, LFA-1, VAP-1
Pro-fibrotic mediators	PDGF, TGF-β

Based on Donate-Correra et al., 2020 [21]; Rayego-Mateos et al., 2020 [22]; Tang et al., 2020 [23]; Vallon et al., 2020 [29]; and Scurt et al., 2019 [30]
Abbreviations: CCL C–C motif ligand, CSF1 colony stimulating factor 1, CXCL chemokine (C-X-C motif) ligand, HMGB1 high mobility group box 1, HSP heat shock protein, ICAM-1 intracellular adhesion molecule, IL interleukin, JAK Janus kinase, LFA-1 lymphocyte function-associated antigen 1, MBL mannose-binding lectin, NLR nucleotide-binding oligomerization domain-like receptor, NLRP3 NACHT LRR and PYD domains-containing protein 3, PDGF platelet-derived growth factor, RAGE receptor for advanced glycation end-products, STAT signal transducer and activator of transcription, TGF-β, transforming growth factor β, TLR toll-like receptor, TNF-α tumor necrosis factor α, VAP-1 vascular adhesion protein 1, VCAM-1 vascular cell adhesion molecule

ISSN: 1471-2369