Special Issue "Redox Stress and Redox Homeostatic Response to Trauma and Injury"
A special issue of Antioxidants (ISSN 2076-3921).
Deadline for manuscript submissions: closed (30 November 2014)
Dr. Nikolai V. Gorbunov
Prompt response to major trauma and injury includes a massive recruitment of numerous mesenchymal, reticuloendotelial, and endothelial precursor cells, along with inflammatory cells from the peripheral blood and the bone marrow in order to sustain the damage recovery. The pathogenesis of trauma/injury is also associated with numerous systemic abnormalities caused by (i) cardiopulmonary, vascular, and neurogenic shock; (ii) the rupturing, hemorrhaging, and edema of internal organs; (iii) progressive systemic hypotension and hypoxia; and (iv) the massive release of paracrine and autocrine factors (e.g., alarmins, DAMPs, nitric oxide, inflammatory cytokines, neurohumoral mediators), and the constituents of damaged cells that drive aseptic inflammation. These events can result in the redox stress, affect redox homeostasis, and suppress cell differentiation and proliferation; thus, these events can exacerbate tissue damage, promote the multiple organ dysfunction syndrome, and/or extend recuperation period in sequelae of the acute diseases.
The Special Issue’s aims and objectives are:
(i) to cover the assessment and integration of the following subjects:
- the interplay between the redox metabolome, redox signaling, and aseptic inflammation that is due to trauma/injury damage to organs and systems
- the advantages and limitations of experimental techniques (including in vitro models) and of the arrays of redox molecular sensors that are employed for assessing traumatic redox stress
(ii) to elucidate the role of “free radical” and “radical-free” mechanisms of redox stress and redox signaling, as well as the effects of antioxidants and other dietary factors in the pathogenesis of aseptic inflammation and post-traumatic recovery.
Prof. Dr. Nikolai V. Gorbunov
Manuscript Submission Information
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- redox/oxidative stress
- redox metabolome
- redox sensors