Mitochondria are essential organelles that control energy synthesis, cell signalling, and apoptosis. Due to their important function in cell metabolism, the quantity and quality of mitochondria must be regulated tightly, through mitochondrial fusion and fission, biogenesis, and degradation. Damaged mitochondria are recycled and degraded through mitophagy, a specific form of selective autophagy. Mitophagy receptors BNIP3(BCL2/adenovirus E1B 19 kDa interacting protein 3) and its homologue BNIP3L (also known as NIX) are mitophagy receptors which tag defective mitochondria and act in concert with the autophagy machinery to engulf damaged mitochondria in the autophagosome double membrane. We have data demonstrating that BNIP3 and BNIP3L are regulated by the Skp1-Cul1-F-box protein (SCF) family of ubiquitin ligases. We are studying the regulatory pathways mediating the degradation of BNIP3 and BNIP3L, as well as the consequence of BNIP3 and BNIP3L stabilisation on cellular mitophagy pathways.