.png){kind=icon}
Return
ROS production by mitochondria: function or dysfunction?
.png){kind=icon}
PRE
AI
DOI：10.1038/s41388-023-02907-z.png)
.png){kind=icon}
Original request for help.png){kind=icon}
Share.png){kind=icon}
Save
Abstract
En 中文
In eukaryotic cells, ATP generation is generally viewed as the primary function of mitochondria under normoxic conditions. Reactive oxygen species (ROS), in contrast, are regarded as the by-products of respiration, and are widely associated with dysfunction and disease. Important signaling functions have been demonstrated for mitochondrial ROS in recent years. Still, their chemical reactivity and capacity to elicit oxidative damage have reinforced the idea that ROS are the products of dysfunctional mitochondria that accumulate during disease. Several studies support a different model, however, by showing that: (1) limited oxygen availability results in mitochondria prioritizing ROS production over ATP, (2) ROS is an essential adaptive mitochondrial signal triggered by various important stressors, and (3) while mitochondria-independent ATP production can be easily engaged by most cells, there is no known replacement for ROS-driven redox signaling. Based on these observations and other evidence reviewed here, we highlight the role of ROS production as a major mitochondrial function involved in cellular adaptation and stress resistance. As such, we propose a rekindled view of ROS production as a primary mitochondrial function as essential to life as ATP production itself.
Keywords:
REGULATES CELL-SURVIVAL
OXIDATIVE DNA-DAMAGE
COMPLEX-III
CYTOCHROME-C
SUPEROXIDE-DISMUTASE
STRESS-RESPONSE
BREAST-CANCER
OXYGEN
APOPTOSIS
KINASE
Journal
IF:
7.3
Papers:
1.9W
Citations:
6.0W
Organization
Cited Papers
TSLP regulates mitochondrial ROS-induced mitophagy via histone modification in human monocytes.png)
CELL AND BIOSCIENCE
OAAI
CELL AND BIOSCIENCEIF6.2
OAAIShareSaveHypoxia-inducible Factor 1α Mediates Anoikis Resistance via Suppression of α5 IntegrinCANCER RESEARCHOAAI
CANCER RESEARCHIF16.6
OAAIShareSaveShareSaveCIB1 prevents nuclear GAPDH accumulation and non-apoptotic tumor cell death via AKT and ERK signalingONCOGENEOAAI
ONCOGENEIF7.3
OAAIShareSaveNon-Hodgkin Lymphoma Risk and Insecticide, Fungicide and Fumigant Use in the Agricultural Health StudyPLoS ONEOAAI
PLoS ONEIF0
OAAIShareSave
View more