A Way in Which Mitochondrial DNA Becomes Misplaced, Provoking Inflammation

Cells respond to the presence of DNA in the cytoplasm with inflammatory signaling, an evolved innate immune response that serves to protect against viral and bacterial infection. This becomes a problem when mitochondria become dysfunctional, as mitochondria contain their own small genome, the mitochondrial DNA. In the context of age-related mitochondrial dysfunction, and a number of other circumstances, fragments of mitochondrial DNA can find their way into the cell cytoplasm. The result is a link between mitochondrial dysfunction and the chronic inflammation of aging, though it remains unclear as to how much of this characteristic unresolved inflammatory signaling is the result of mislocated DNA versus, say, the presence of senescent cells, or other contributions. Is there something that can be done to block this unwanted inflammatory signaling, short of repairing or replacing dysfunctional mitochondria throughout the body? Perhaps, perhaps not, but further research is the only way to find out. Mitochondrial DNA (mtDNA) encodes essential subunits of the oxidative phosphorylation system, but is also a major damage-associated molecular pattern (DAMP) that engages innate immune sensors when released into the cytoplasm, outside of cells or into circulation. As a DAMP, mtDNA not only contributes to anti-viral resistance, but also causes pathogenic inflammation in many disease contexts. Cells experiencing mtDNA stress caused by depletion of the mtDNA-packaging protein, mi...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs