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2017 ; 8
(ä): 296
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Functional Mitochondria in Health and Disease
#MMPMID29163365
Herst PM
; Rowe MR
; Carson GM
; Berridge MV
Front Endocrinol (Lausanne)
2017[]; 8
(ä): 296
PMID29163365
show ga
The ability to rapidly adapt cellular bioenergetic capabilities to meet rapidly
changing environmental conditions is mandatory for normal cellular function and
for cancer progression. Any loss of this adaptive response has the potential to
compromise cellular function and render the cell more susceptible to external
stressors such as oxidative stress, radiation, chemotherapeutic drugs, and
hypoxia. Mitochondria play a vital role in bioenergetic and biosynthetic pathways
and can rapidly adjust to meet the metabolic needs of the cell. Increased demand
is met by mitochondrial biogenesis and fusion of individual mitochondria into
dynamic networks, whereas a decrease in demand results in the removal of
superfluous mitochondria through fission and mitophagy. Effective communication
between nucleus and mitochondria (mito-nuclear cross talk), involving the
generation of different mitochondrial stress signals as well as the nuclear
stress response pathways to deal with these stressors, maintains bioenergetic
homeostasis under most conditions. However, when mitochondrial DNA (mtDNA)
mutations accumulate and mito-nuclear cross talk falters, mitochondria fail to
deliver critical functional outputs. Mutations in mtDNA have been implicated in
neuromuscular and neurodegenerative mitochondriopathies and complex diseases such
as diabetes, cardiovascular diseases, gastrointestinal disorders, skin disorders,
aging, and cancer. In some cases, drastic measures such as acquisition of new
mitochondria from donor cells occurs to ensure cell survival. This review starts
with a brief discussion of the evolutionary origin of mitochondria and summarizes
how mutations in mtDNA lead to mitochondriopathies and other degenerative
diseases. Mito-nuclear cross talk, including various stress signals generated by
mitochondria and corresponding stress response pathways activated by the nucleus
are summarized. We also introduce and discuss a small family of recently
discovered hormone-like mitopeptides that modulate body metabolism. Under
conditions of severe mitochondrial stress, mitochondria have been shown to
traffic between cells, replacing mitochondria in cells with damaged and
malfunctional mtDNA. Understanding the processes involved in cellular
bioenergetics and metabolic adaptation has the potential to generate new
knowledge that will lead to improved treatment of many of the metabolic,
degenerative, and age-related inflammatory diseases that characterize modern
societies.
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