2013
DOI: 10.1089/ars.2011.4357
|View full text |Cite
|
Sign up to set email alerts
|

Mitoplasticity: Adaptation Biology of the Mitochondrion to the Cellular Redox State in Physiology and Carcinogenesis

Abstract: Adaptation and transformation biology of the mitochondrion to redox status is an emerging domain of physiology and pathophysiology. Mitochondrial adaptations occur in response to accidental changes in cellular energy demand or supply while mitochondrial transformations are a part of greater program of cell metamorphosis. The possible role of mitochondrial adaptations and transformations in pathogenesis remains unexplored, and it has become critical to decipher the stimuli and the underlying molecular pathways.… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

0
35
0

Year Published

2014
2014
2020
2020

Publication Types

Select...
5
2
1

Relationship

0
8

Authors

Journals

citations
Cited by 38 publications
(35 citation statements)
references
References 283 publications
0
35
0
Order By: Relevance
“…The fact that it is also consistently differentially expressed may indicate that the COI gene, and potentially other mitochondrial genes, may be the original target of selection between the strains (Meiklejohn, Montooth, and Rand 2007). Changes in mitochondrial functions are associated to changes in energy demand or supply (Jose et al 2013). In addition, variations in mitochondrial sequences can be the cause of mitonuclear incompatibilities between species (Hill 2015).…”
Section: Cc-by-nc-ndmentioning
confidence: 99%
“…The fact that it is also consistently differentially expressed may indicate that the COI gene, and potentially other mitochondrial genes, may be the original target of selection between the strains (Meiklejohn, Montooth, and Rand 2007). Changes in mitochondrial functions are associated to changes in energy demand or supply (Jose et al 2013). In addition, variations in mitochondrial sequences can be the cause of mitonuclear incompatibilities between species (Hill 2015).…”
Section: Cc-by-nc-ndmentioning
confidence: 99%
“…This may either be the result of increased energy expenditure such as with endurance training, or due to a functional mitochondrial defect or mutation, relevant during pathological conditions. During energy crisis, ATP deficiency and/or mitochondrial dysfunction will activate adaptive mechanisms attempting to counterbalance this situation [23,24,[42][43][44]. These interlinked regulatory systems control mitochondrial content at the transcriptional and functional level by modulating mitochondrial biogenesis/degradation, fission/fusion dynamics, motility and/or respiration [23].…”
Section: Regulation Of Mitochondrial Contentmentioning
confidence: 99%
“…During energy crisis, ATP deficiency and/or mitochondrial dysfunction will activate adaptive mechanisms attempting to counterbalance this situation [23,24,[42][43][44]. These interlinked regulatory systems control mitochondrial content at the transcriptional and functional level by modulating mitochondrial biogenesis/degradation, fission/fusion dynamics, motility and/or respiration [23]. Of note, mitochondrial content modulation might not work identically in the various cell types because of their different biological function and mitochondrial morphology (Fig.…”
Section: Regulation Of Mitochondrial Contentmentioning
confidence: 99%
See 1 more Smart Citation
“…18 A growing body of evidence indicates that mitochondrial network morphology and function are closely connected in active metabolic cells, particularly in cardiomyocytes. 19 Yu et al 20 showed that hyperglycemia leads to Drp1-induced mitochondrial fission in neonatal rat ventricular myocytes, which in turn induced mitochondrial dysfunction and proapoptotic pathway activation. In agreement, Shenouda et al 21 showed that hyperglycemia alters the expression of proteins implicated in mitochondrial dynamics, that is, increased expression of FIS1 and DRP1 proteins, and induces mitochondrial fragmentation in human endothelial cells.…”
mentioning
confidence: 99%