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The OPA1-dependent mitochondrial cristae remodeling pathway controls atrophic,
apoptotic, and ischemic tissue damage
#MMPMID26039448
Varanita T
; Soriano ME
; Romanello V
; Zaglia T
; Quintana-Cabrera R
; Semenzato M
; Menabò R
; Costa V
; Civiletto G
; Pesce P
; Viscomi C
; Zeviani M
; Di Lisa F
; Mongillo M
; Sandri M
; Scorrano L
Cell Metab
2015[Jun]; 21
(6
): 834-44
PMID26039448
show ga
Mitochondrial morphological and ultrastructural changes occur during apoptosis
and autophagy, but whether they are relevant in vivo for tissue response to
damage is unclear. Here we investigate the role of the optic atrophy 1
(OPA1)-dependent cristae remodeling pathway in vivo and provide evidence that it
regulates the response of multiple tissues to apoptotic, necrotic, and atrophic
stimuli. Genetic inhibition of the cristae remodeling pathway in vivo does not
affect development, but protects mice from denervation-induced muscular atrophy,
ischemic heart and brain damage, as well as hepatocellular apoptosis.
Mechanistically, OPA1-dependent mitochondrial cristae stabilization increases
mitochondrial respiratory efficiency and blunts mitochondrial dysfunction,
cytochrome c release, and reactive oxygen species production. Our results
indicate that the OPA1-dependent cristae remodeling pathway is a fundamental,
targetable determinant of tissue damage in vivo.
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