About this Research Topic
Mitochondria are essential organelles for neuronal function and survival. By regulating energy metabolism, calcium buffering, signal transduction, synaptic development, and plasticity, mitochondria ensure effective communication and energy availability throughout the full extension of neuronal cells. These functions could not be exerted without the fundamental dynamic balance between mitochondrial fusion and fission, and mitochondrial selective elimination through mitophagy. Alterations in mitochondrial functionality are known to cause neuronal damage and death.
Many neurotoxins are prone to affect mitochondrial function. They can accumulate inside the organelle or affect its dynamics. By disrupting mitochondrial complex activity and morphology, neurotoxins trigger detrimental oxidative stress and damage mitochondrial DNA integrity, finally leading to mitochondria-related apoptosis, necrosis, and autophagy. Some neurotoxins are also known to affect mitochondrial fusion-fission balance and motility. For example, cadmium was shown to cause increased mitochondrial fragmentation, activation of the transcription factor EB-dependent autophagy and impairment of lysosomal-mitochondrial axis.
By targeting mitochondrial proteins expression, several compounds or active substances from plant extracts have certain protective effects against the detrimental toxicity of neurotoxins. For example, it was shown that administration of Melatonin or Auraptene (an extract from citrus fruit) ameliorates neurotoxin-induced oxidative stress in dopaminergic neurons and increases the expression of antioxidant enzymes in MPTP-induced PD mouse model.
Mitochondria gained growing attention as neurotoxins' targets. Therefore, elucidating the mechanism underlying this toxicity could lead to potential therapeutic strategies.
The aim of this Research Topic is to gather original articles that further elucidate the mechanism caused by neurotoxins. This could lead to various mitochondrial dysfunction including, but not limited to, mt-DNA oxidative damage, impairment of mitophagy, and fusion-fission imbalance. A better understanding of these mechanisms might allow the discovering of new therapeutic targets involved in mitochondrial DNA maintenance, mitochondrial dynamics and mitochondrial protein quality control.
Keywords: Neurotoxicity, oxidative stress, mitochondrial DNA, mitophagy, mitochondrial dynamics
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