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Fig. 1 | Journal of Translational Medicine

Fig. 1

From: The pathogenesis of renal injury and treatment in light chain deposition disease

Fig. 1

The interaction between light chain deposition disease (LCDD) free light chain (FLCs) and mesangial cells (MCs): FLCs enter MCs through a putative receptor. LCDD FLCs are processed in endosomes. The processed FLCs are deposited on the membrane of mesangial cells as granular deposits. Meanwhile, transforming growth factor (TGF)-β production is increased and matrix metalloproteinase (MMP)-7 is decreased, resulting in an increase in ECM and tenascin. Furthermore, TGF-β leads to apoptosis and the late deletion of cells. Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), as a dimer of P50 and p65 subunits, usually exists in the cytoplasm of MCs, binding to its inhibitor protein, IκB. When LCs stimulate MCs, IκB is released from the dimer, resulting in NF-κB migration to the nucleus. NF-κB binds to specific DNA (MCP-1, RANTES, ICAM-1), leading to inflammatory cell infiltration and an increase MCP-1. The functional interaction between NF-κB and SMAD leads to the activation of COL7A1 expression, resulting in an increase in ECM. Ribosomal S6 kinase (RSK) phosphorylates c-fos. Then the activation of c-fos results in the transcription of PDGF-β. PDGF induces MCs to be exposed to monoclonal LC, and cell surface wrinkling increases the cell surface area and promotes MC early proliferation. LCDD Light chain deposition disease, FLC Free light chain, ECM Extracellular matrix, TGF-β Transforming growth factor-β, MMP-7 Matrix metalloproteinases-7, RSK Ribosomal S6 kinase, NF-κB Nuclear factor kappa-light-chain-enhancer of activated B cells, PDGF Platelet-derived growth factor, MCP Monocyte chemoattractant protein, RANTES Regulated upon activation normal T-expressed and secreted, ICAM-1 Intercellular adhesion molecule-1

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