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2017 ; 13
(6
): 1080-1081
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English Wikipedia
Mitophagy receptor FUNDC1 regulates mitochondrial homeostasis and protects the
heart from I/R injury
#MMPMID28323531
Zhang W
; Siraj S
; Zhang R
; Chen Q
Autophagy
2017[Jun]; 13
(6
): 1080-1081
PMID28323531
show ga
Mitophagy plays pivotal roles in the selective disposal of unwanted mitochondria,
and accumulation of damaged mitochondria has been linked to aging-related
diseases. However, definitive proof that mitophagy regulates mitochondrial
quality in vivo is lacking. It is also largely unclear whether damaged
mitochondria are the cause or just the consequence of these diseases. We
previously showed that FUNDC1 is a mitophagy receptor that interacts with LC3 to
mediate mitophagy in response to hypoxia in cultured cells. We established Fundc1
knockout mouse models and used genetic and biochemical approaches, including a
synthetic peptide that blocks the FUNDC1-LC3 interaction, to demonstrate that
mitophagy regulates both mitochondrial quantity and quality in vivo in response
to hypoxia or hypoxic conditions caused by ischemia-reperfusion (I/R) heart
injury. We found that hypoxic mitophagy regulates platelet activities.
Furthermore, we found that hypoxic preconditioning induces FUNDC1-dependent
mitophagy in platelets and reduces I/R-induced heart injury, suggesting a new
strategy to protect cardiac function and fight cardiovascular diseases.