Participation of parkin in the molecular mechanisms of inflammasome activation in human myelo- and lymphoid leukemia lines

Chronic inflammation plays a key role in the development and course of neoplastic diseases of the hematopoietic system, including myeloid and lymphoid leukemias. Recent reports suggest that excessive and uncontrolled activation of a protein structure called the inflammasome may be a determinant of chronic inflammation. Strong activators of the inflammasome include reactive oxygen species resulting from dysfunction and / or life cycle of the mitochondria, danger associated molecular patterns (DAMPs) and ATP. Function, life cycle and mitochondrial degradation through mitophagy are regulated by parkin, an enzyme essential for the proper functioning of the ubiquitin-proteasome system. Literature data show that the activity of parkin is regulated, among others, by caspase 1, and oxidative stress-dependent deregulation of parkin is associated with the accumulation of non-functional mitochondria in cells. Determining the importance of parkin in the molecular mechanisms of inflammasome activation will significantly influence further research on the development of a method of inhibiting parkin-related mitochondrial dysfunction, thus preventing excessive activation of the inflammasome and the development of neoplastic diseases of the hematopoietic system.