There are many unsolved enigmas on the link between mitochondrial activity and inflammation. One of the processes that were described so far reveals that the accumulation of faulty mitochondria can lead to inflammatory processes. Now, a scientific team has found out that the removal of Opa1, the mitochondrial protein, in a mouse muscle, generates a general inflammatory process that is able to cause premature death to the animal. The study, published in The EMBO Journal, is led by Antonio Zorzano, professor at the Faculty of Biology of the UB, head of the group at the Institute for Research in Biomedicine (IRB Barcelona) and the Diabetes and Associated Metabolic Diseases Networking Biomedical Research Centre (CIBERDEM).

Mitochondria are the cell organs running the energy metabolism of the cell, and are especially abundant in the muscle and the liver. These cell components adjust, split, expand, and shrink constantly, in an active process known as mitochondrial dynamics. In this process, some proteins, such as Opa1 and Mitofusin 1 and 2, take part in the merging of internal membranes of mitochondria.

The new study explains that the removal of the protein Opa 1 in the muscle fiber of the musculoskeletal generates an acute inflammatory process that is transferred from the muscle fiber to the whole body. This inflammatory response causes growth to stop and it has an impact on the animal’s longevity. According to Professor Antonio Zorzano, “this is the first time we noticed a lack of a muscular mitochondrial protein that can generate such a big inflammatory response; these findings give us more information on the link between mitochondria and inflammation.”

The new research study provides new perspectives on the potential origin of some inflammatory diseases that could be related to alterations in mitochondrial proteins.