Related Experiment Video
Updated: Aug 1, 2025
Ratiometric Biosensors that Measure Mitochondrial Redox State and ATP in Living Yeast Cells
Published on: July 22, 2013
How the Disruption of Mitochondrial Redox Signalling Contributes to Ageing
Beatriz Castejon-Vega1, Mario D Cordero1,2, Alberto Sanz1
1School of Molecular Biosciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK.
Abstract:
In the past, mitochondrial reactive oxygen species (mtROS) were considered a byproduct of cellular metabolism. Due to the capacity of mtROS to cause oxidative damage, they were proposed as the main drivers of ageing and age-related diseases. Today, we know that mtROS are cellular messengers instrumental in maintaining cellular homeostasis. As cellular messengers, they are produced in specific places at specific times, and the intensity and duration of the ROS signal determine the downstream effects of mitochondrial redox signalling. We do not know yet all the processes for which mtROS are important, but we have learnt that they are essential in decisions that affect cellular differentiation, proliferation and survival. On top of causing damage due to their capacity to oxidize cellular components, mtROS contribute to the onset of degenerative diseases when redox signalling becomes dysregulated. Here, we review the best-characterized signalling pathways in which mtROS participate and those pathological processes in which they are involved. We focus on how mtROS signalling is altered during ageing and discuss whether the accumulation of damaged mitochondria without signalling capacity is a cause or a consequence of ageing.
Insights
Mitochondrial reactive oxygen species (mtROS) are vital cellular messengers, not just damaging byproducts. Dysregulated mtROS signalling contributes to aging and disease, highlighting their complex role in cellular health and pathology.
Area of Science:
- Cellular Biology
- Mitochondrial Function
- Redox Signalling
Background:
- Mitochondrial reactive oxygen species (mtROS) were historically viewed as metabolic byproducts causing cellular damage and driving aging.
- Emerging evidence establishes mtROS as crucial cellular messengers regulating homeostasis, differentiation, proliferation, and survival.
- Dysregulation of mtROS signalling is implicated in age-related and degenerative diseases.
Purpose of the Study:
- To review characterized signalling pathways involving mtROS.
- To explore pathological processes linked to mtROS.
- To examine alterations in mtROS signalling during aging and its relationship with mitochondrial damage.
Main Methods:
- Literature review of established signalling pathways involving mtROS.
- Analysis of pathological processes associated with mtROS dysregulation.
- Discussion of the role of mtROS signalling in the aging process.
Main Results:
- mtROS function as essential signalling molecules, not merely damaging agents.
- Specific mtROS signalling pathways are crucial for cellular fate decisions.
- Altered mtROS signalling contributes to degenerative diseases and aging.
Conclusions:
- mtROS are critical for cellular homeostasis and fate decisions.
- Dysregulated mtROS signalling is a key factor in aging and disease pathogenesis.
- The relationship between mitochondrial damage accumulation and aging requires further investigation.
Related Concept Videos
01:37Mitochondria
01:46Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
01:45Mitochondrial Membranes
01:19Translocation of Proteins into the Mitochondria
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
01:43Electron Transport Chain: Complex III and IV
01:26Aging
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...