Cystogenesis by Jong Hoon Park, Curie Ahn (eds.)

By Jong Hoon Park, Curie Ahn (eds.)

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2015; Gregory et al. 2006). In addition, pro-inflammatory cytokines are up-regulated in PKD. It was reported that an increased concentration of TNF-α induces inflammation and proliferation (Li et al. 2008; Ta et al. 2013). TGFβ, MMPs, and TIMPs trigger fibrosis, especially TGF-β, which is involved in fibrosis as an inflammatory cytokine. MMPs and TIMPs induce the re-structuring of cell formations and the accumulation of collagen and fibroblasts. An increase in the abundance of cytokines and growth factors can lead to the development of inflammation and fibrosis.

NF-kB is a transcription factor that is involved in cell survival and the immune response. In canonical NF-kB signaling, when NF-kB is stimulated by factors such as TNF-α, IL-2, or lymphocytes, activated IKK complex phosphorylates IkB proteins, leading to polyubiquitination. Ubiquitinated IkB is degraded by the proteasome, freeing the p50/p65 NF-kB dimer to translocate to the nucleus and activate gene transcription (Skaug et al. 2009; Gilmore 2006; Jost and Ruland 2007). NF-kB regulates pro-inflammatory cytokines including TNF-α, IL-1α, CCL3, CCL4, and MCP1 (Tak and Firestein 2001).

However, inflammation and fibrosis alone are not able to generate PKD, which also requires hyper-proliferation to occur in the kidneys. Following an increase in cell proliferation, the abundance of certain cells and cytokines is elevated. Macrophage and cytokines secreted by macrophages accumulate in cysts and urine (Swenson-Fields et al. 2013; Zheng et al. 2003; Cowley et al. 2001; Chen et al. 2015; Gregory et al. 2006). In addition, pro-inflammatory cytokines are up-regulated in PKD. It was reported that an increased concentration of TNF-α induces inflammation and proliferation (Li et al.

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