Inhibition of Oxidative Stress and Related Signaling Pathways in Neuroprotection
A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".
Deadline for manuscript submissions: closed (30 September 2023) | Viewed by 17692
2. School of Medicine, Catholic University of Croatia, 10000 Zagreb, Croatia
Interests: neuropharmacology; phytopharmaceuticals; oxidative stress; neuroprotection; neurodegenerative diseases
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As the world’s population is getting older, neurodegenerative diseases, such as Alzheimer’s and Parkinson’s disease, represent a growing medical, economic, and social threat. The progressive loss of neuronal cells in vulnerable brain areas is the most prominent hallmark of neurodegenerative diseases. Oxidative stress is one of the major underlying mechanisms of neuronal death. It also drives other molecular and cellular mechanisms that exacerbate the detrimental consequences of redox imbalance. These include excitotoxicity, endoplasmic reticulum stress and the disturbance of calcium homeostasis, the alteration of the brain lipid profile, and the impairment of mitochondrial function and protein aggregation, to mention the most important ones, which are followed by pronounced inflammation, gliosis, axonal degeneration, the impairment of synaptic transmission, and ultimately, neuronal death.
Oxidative stress can be the initiating factor in the activation of various redox-sensitive signalling pathways which are highly implicated in the onset and progression of molecular and cellular mechanisms driving neurodegeneration. Several transcription factors, including Nrf2, PPARγ, NF- κB and p53, are particularly important in tuning antioxidative activity, inflammatory responses and neuronal death or survival upon the disruption of redox balance. The activation of MAP kinases ERK1/2, JNK and p38, together with the activation of the Akt/PKB pathway and its downstream effector PI-3K, also plays an important role in the neuronal response to oxidative stress and neuroprotection. The contribution of lipid signalling pathways in neurodegenerative diseases is slowly beginning to be elucidated.
Unfortunately, although considerable progress has been made towards understanding the pathological mechanisms involved in neurodegeneration, this knowledge has not yet been successfully translated into clinics. Current therapeutic options are limited and bring only a temporary relief from the symptoms. As oxidative stress is highly involved in various pathological processes accompanying neurodegeneration, pharmacological strategies focused on the prevention or attenuation of oxidative injury are considered as relevant approaches in neuroprotection. Various phytochemicals, as well as other natural and synthetic compounds, capable of regaining redox homeostasis and attenuating the oxidative stress-induced modulation of intracellular signalization in injured neurons, could represent valuable research avenues in neuroprotection.
The Special Issue entitled “Inhibition of Oxidative Stress and Related Signaling Pathways in Neuroprotection” is hence devoted to gathering the latest findings covering novel neuroprotective niches in in vitro and in vivo settings that prevent or delay neuronal loss by targeting oxidative stress and related signalling pathways. Hopefully, a better understanding of cellular and molecular mechanisms of action of neuroprotective compounds along intracellular signalling cascades may pave the way toward effective therapies that are eagerly awaited.
Dr. Maja Jazvinšćak Jembrek
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- oxidative stress
- signalling pathways
- neuroprotective drugs
- mitochondrial function