Publication details
Impaired mitophagy in Fanconi anemia is dependent on mitochondrial fission
| Authors | |
|---|---|
| Year of publication | 2016 |
| Type | Article in Periodical |
| Magazine / Source | Oncotarget |
| MU Faculty or unit | |
| Citation | |
| Doi | http://dx.doi.org/10.18632/oncotarget.11161 |
| Field | Genetics and molecular biology |
| Keywords | mitophagy; impaired autophagy; Fanconi anemia; ROS; oxidative stress |
| Attached files | |
| Description | Fanconi anemia (FA) is a rare genetic disorder associated with bone-marrow failure, genome instability and cancer predisposition. Recently, we and others have demonstrated dysfunctional mitochondria with morphological alterations in FA cells accompanied by high reactive oxygen species (ROS) levels. Mitochondrial morphology is regulated by continuous fusion and fission events and the misbalance between these two is often accompanied by autophagy. Here, we provide evidence of impaired autophagy in FA. We demonstrate that FA cells have increased number of autophagic (presumably mitophagic) events and accumulate dysfunctional mitochondria due to an impaired ability to degrade them. Moreover, mitochondrial fission accompanied by oxidative stress (OS) is a prerequisite condition for mitophagy in FA and blocking this pathway may release autophagic machinery to clear dysfunctional mitochondria. |