Cellular and Molecular Mechanisms of Oxidative Stress in Nerve Injury
1Southern Medical University, Guangzhou, China
2University of Hong Kong, Hong Kong
3Massachusetts General Hospital - Harvard Medical School, Boston, USA
Cellular and Molecular Mechanisms of Oxidative Stress in Nerve Injury
Description
Due to the importance of neurons and the nervous system, neurological injury-related diseases (such as stroke, spinal cord injury, peripheral nerve injury, and neuropathic injury) have attracted more and more attention. Neurons are highly susceptible to damage and dead neuronal cells are non-regenerable; consequently, nerve injury is difficult to repair. Research concerning the pathophysiological process and related mechanisms after nerve injury is important for preventing and treating neurological injury-related diseases and pathological changes.
Oxidative stress has been an important area of research for many years, as it is of vital importance to physiology, pathophysiology, and clinical aspects. It is well known that oxidative stress plays an important role in normal physiological functions (e.g., cellular and molecular signalling pathways, especially in the nervous system) and in the prevention and treatment of neurological diseases. Oxidative stress is one of the important factors and mechanisms that regulates the normal physiological functions of nerve cells and can cause changes in many molecular signalling pathways. The understanding of the complex and convoluted relationship between oxidative stress and nervous system (dys)function with pathophysiological and functional consequences, from a molecular and cellular level to tissue and organ levels, represents a major challenge. The understanding of these interactions is, however, crucial if we want to develop effective treatments for neurological injuries and disorders of the nervous system.
The aim of this Special Issue is to focus on oxidative stress as a potential initiating pathological and physiological factor in nerve injury-related diseases and pathology. This is an important topic as increasing evidence suggests that oxidative stress plays an important role after nerve injury and could be a target for the treatment of such injuries. This Special Issue welcomes the latest research findings on apoptosis, autophagy, hypoxia-ischemic injury, inflammatory injury, neurohumoral imbalance, and other functional damages in vivo and in vitro studies of nerve injury, as well as the latest research in proteomics and genomics in the nervous system. Clinical, basic, and translational medicine research is welcome, as well as review articles.
Potential topics include but are not limited to the following:
- Pathophysiology of oxidative stress as a cause and perpetuating factor of nerve injury
- Cellular molecular basis and mechanisms of oxidative stress in nerve injury
- Oxidative stress as a therapeutic target in nerve injury
- Oxidative stress mediated neuro-immune inflammatory response in nerve damage
- The mechanism and repairing of oxidative stress caused damage to neuronal organelles such as DNA, mitochondria, and endoplasmic reticulum