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191 In diabetic wounds, excessive NET formation triggers activation of the NOD-like receptor protein 3 (NLRP3) inflammasome and induces the release of IL-1 in macrophages via the TLR-4/TLR-9/ nuclear factor enhancer of activated B cells (NF-B) signaling pathway

In vivo and ex vivo studies in animal models of MS have shown that the pro-inflammatory cytokines IL-1, TNF- and IL-18 are involved in the synaptic loss of the disease, which may occur independently of demyelination and neuronal degeneration (148)

The depletion of FUNDC1 levels in CC cell lines, particularly HeLa and Caski cells, leads to a reduction in the expression of the anti-apoptotic protein BCL2L1

PMID: 16702333 | DOI: 10.1093/jn/136.6.1636S [13] Kumar P, Osahon OW, Vides DB, et al

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