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. 2025 Jul 24;21(11):4762–4781. doi: 10.7150/ijbs.114907

Table 2.

Crosstalk between MCs and other cells in DKD

Cell Types Mediators or Related Pathways Effects Reference(s)
GECs → MCs PDGF-B/PDGFR-β signaling pathways Promoting the proliferation of MCs and aggravating the progression of DKD 127
GECs → MCs TGFβ1/Smad3 signaling Mediating MCs proliferation and increased matrix protein production 130
MCs→ GECs Integrin αvβ8/TGF-β Inhibiting TGF-β-mediated damage in endothelial cells 128
GECs → MCs ET-1/ETAR Promoting MCs proliferation and ECM accumulation 132
GECs → MCs LRG1 Overactivating TGF-β and driving the progression of DKD. 141
MCs→ GECs SLIT2/ROBO1 Promoting GECs aberrant intraglomerular angiogenesis 144
MCs→ podocytes TGFβ1/PI3K-AKT signaling pathway Induced podocytes apoptosis 122
MCs→ podocytes Endoplasmic reticulum (ER)-associated degradation (ERAD) Inhibiting of ERAD-related proteins, inducing podocyte apoptosis, and promoting the progression of DKD 198
PTECs → MCs miR-92a-1-5p Promoting endoplasmic reticulum stress and myofibroblast cell transdifferentiation (MFT) in MCs 151
Macrophages → MCs TGF-β1/Smad3 signaling pathway Promoting the proliferation of MCs and the progression of DKD 154
Macrophages → MCs NLRP3 inflammasome Activating of NLRP3 inflammasome and inhibiting MC autophagy 158