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Systemic regulation of mitochondrial stress
Systemic regulation of mitochondrial stress
Mitochondria play vital roles in the processes of aging and maintaining healthspan. In the model organism C. elegans, it has been observed that mitochondrial dysfunction in one organ can impact the mitochondrial stress response pathway in remote tissues. Building upon this observation, our research aims to delve into the consequences of mitochondrial dysfunction in a specific subset of neurons and its influence on overall organismal aging and healthspan.
Mitochondrial Function in Neuronal Aging
The positioning and function of mitochondria in neurons are regulated by intricate interactions that govern the delicate balance of processes such as fission/fusion, trafficking, targeting, anchoring, and quality control. Extensive research has focused on identifying key factors involved in each of these processes. However, there are still gaps in our understanding of how these intricate mitochondrial changes are coordinated to maintain mitochondrial localization and function at specific regions within neurons, including synapses and axons, under normal conditions. Furthermore, the impact of aging and age-related diseases on these processes remains to be fully elucidated.
Mitochondrial Function in the Recovery of Injured Neurons
Mitochondria undergo dynamic changes in their morphology, motility, number, and activity to match local energy demand and maintain cellular homeostasis. These changes include processes such as fusion and division. Recent studies conducted by our research team, as well as other researchers, using young model animals, have revealed the critical role of mitochondrial dynamics and activity in determining the capacity for axon regeneration following axonal injury. Furthermore, mounting evidence suggests that aging significantly increases the risk of mitochondrial abnormalities within the nervous system.
Our research aims to investigate the role of mitochondria in axon regeneration of adult neurons during aging.
By delving into these areas, we hope to gain a deeper understanding of how mitochondrial function influences the recovery of injured neurons, particularly in the context of aging.
GABA motor neuron 24 after axotomy. Axon injury increases mitochondrial density
Arrowheads indicate mito::mCherry. Aritesks indicate the proximal tip of injured axon.
Regulation of Gene Expression During Axon Regeneration and Aging in Neurons
The process of axon regeneration in neurons is highly dependent on the regulation of gene expression within the damaged neurons. While some signaling pathways that control the transcriptional changes in injured neurons have been identified, our understanding of how these neurons regulate gene expression at the post-transcriptional level to influence axon regeneration remains limited. Additionally, the mechanisms governing gene expression regulation during aging in neurons continue to be a topic of ongoing research.
Mitochondrial Response to Environmental Toxicants
Mitochondria serve as crucial intracellular targets for a wide range of environmental toxicants, including pollutants, heavy metals, and pesticides. Exposure to these toxins, whether over a short or long duration, can elicit substantial alterations in mitochondrial morphology, dynamics, physiological properties, activity, homeostasis, and interplay with other intracellular organelles. Importantly, the resulting mitochondrial dysfunction caused by environmental toxicity can have significant implications for an organism's overall health and survival.
To investigate the effects of environmental contaminants on mitochondria and their subsequent impact on an organism's well-being and lifespan, we employ the nematode C. elegans as an in vivo model. Through this model system, we can assess and elucidate the mechanisms underlying mitochondrial responses to environmental toxicants and their consequences.
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