Damaged mitochondria are recognised by PTEN-induced putative kinase-1 (PINK1), which recruits Parkin, leading to ubiquitination (Ub) and engulfment into an autophagosome through binding to autophagy receptors (AR), such as p62, which binds to LC3-II. Fusion with a lysosome leads to degradation and removal of defective mitochondria in healthy cells. In COPD, Parkin is reduced so defective mitochondria accumulate in cells and may fuse and branch and release mitochondrial reactive oxygen species (mROS) and mitochondrial (mt)DNA.