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2015 ; 11
(8
): 1428-30
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Coupling mitogenesis and mitophagy for longevity
#MMPMID26083448
Palikaras K
; Lionaki E
; Tavernarakis N
Autophagy
2015[]; 11
(8
): 1428-30
PMID26083448
show ga
Maintenance of mitochondrial function and energy homeostasis requires both
generation of newly synthesized and elimination of dysfunctional mitochondria.
Impaired mitochondrial function and excessive mitochondrial content are major
characteristics of aging and several human pathophysiological conditions,
highlighting the pivotal role of the coordination between mitochondrial
biogenesis and mitophagy. However, the cellular and molecular underpinnings of
mitochondrial mass homeostasis remain obscure. In our recent study, we
demonstrate that DCT-1, the Caenorhabditis elegans homolog of mammalian BNIP3 and
BNIP3L/NIX, is a key mediator of mitophagy promoting longevity under stress.
DCT-1 acts downstream of the PINK-1-PDR-1/Parkin pathway and is ubiquitinated
upon mitophagy-inducing conditions to mediate the removal of damaged
mitochondria. Accumulation of damaged mitochondria triggers SKN-1 activation,
which initiates a bipartite retrograde signaling pathway stimulating the
coordinated induction of both mitochondrial biogenesis and mitophagy genes. Taken
together, our results unravel a homeostatic feedback loop that allows cells to
adjust their mitochondrial population in response to environmental and
intracellular cues. Age-dependent decline of mitophagy both inhibits removal of
dysfunctional or superfluous mitochondria and impairs mitochondrial biogenesis
resulting in progressive mitochondrial accretion and consequently, deterioration
of cell function.
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