Mitochondrial Stress Provokes Inflammation via Fragments of Mitochondrial DNA

A large body of evidence links mitochondrial dysfunction with chronic inflammation. These are both features of aging, but it appears that dysfunctional, stressed mitochondria are a meaningful cause of inflammatory signaling. Mitochondria can generate molecular fragments, such as pieces of mitochondrial DNA, that are recognized as potentially threatening by the innate immune system. These damage-associated molecular patterns are present in much greater amounts in old tissues, and the immune system reacts to them to produce lasting, unresolved inflammation, harmful to tissue function rather than protective. In today's research materials, scientists report on their investigation of how exactly it is that mitochondrial DNA fragments are ejected from cells to then provoke an immune response. Understanding the details of the processes involved may reveal points of intervention that can be used to suppress age-related chronic inflammation. The researchers here suggest FEN1 inhibition as a possibility, as this protein is involved in producing the fragments of DNA that then exit the cell to act as damage-associated molecular patterns. How Mitochondrial Damage Ignites the "Auto-Inflammatory Fire" When stressed, damaged or dysfunctional, mitochondria expel their DNA (mtDNA), oxidized and cleaved, into the cytosol - the fluid within a cell in which organelles float - and beyond into the bloodstream, triggering inflammation. In autoimmune conditions like lupus and r...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs