Figure 1.

Mitochondrial dysfunction associated with IBD. Pro-inflammatory cytokines and bacterial toxins are implicated in mitochondrial alterations during IBD. Decreased activity of ETC complexes, decreased ATP levels, accumulation of mtROS, accumulation of misfolded or unfolded proteins in the matrix, and ultrastructural changes such as dissolved cristae have been reported in mitochondria of the epithelium of IBD patients. Subsequent loss of epithelial barrier integrity, epithelial cell apoptosis, and bacterial invasion have been demonstrated following mitochondrial dysfunction in the epithelium. mtDNA is released into the serum of IBD patients and serves as a DAMP for immune cell activation. Additionally, damaged mitochondria can signal inflammasome activation, leading to pro-inflammatory cytokine production.